Library homepage

  • school Campus Bookshelves
  • menu_book Bookshelves
  • perm_media Learning Objects
  • login Login
  • how_to_reg Request Instructor Account
  • hub Instructor Commons
  • Download Page (PDF)
  • Download Full Book (PDF)
  • Periodic Table
  • Physics Constants
  • Scientific Calculator
  • Reference & Cite
  • Tools expand_more
  • Readability

selected template will load here

This action is not available.

Chemistry LibreTexts

10.1: The Krebs Cycle (Citric Acid Cycle)

  • Last updated
  • Save as PDF
  • Page ID 167348

The primary catabolic pathway in the body is the  citric acid cycle (CAC)  because it is here that oxidation to CO 2  occurs for breakdown products of the cell’s major building blocks - sugars, fatty acids, amino acids. The pathway is cyclic ( Figure 10.1 ) and thus, doesn’t really have a starting or ending point. All of the reactions occur in the mitochondrion, though one enzyme is embedded in the organelle’s membrane. As needs change, cells may use a subset of the reactions of the cycle to produce a desired molecule rather than to run the entire cycle.

The primary catabolic pathway in the body is the citric acid cycle, also known as the tricarboxylic acid cycle and the Krebs cycle, completes the oxidation of glucose by taking the pyruvates from  glycolysis  (and other pathways), and completely breaking them down into CO 2  molecules, H 2 O molecules, and generating additional ATP by oxidative phosphorylation. In prokaryotic cells, the citric acid cycle occurs in the cytoplasm; in eukaryotic cells the citric acid cycle takes place in the matrix of the mitochondria.

The overall reaction for the citric acid cycle is :

     2 acetyl groups + 6 NAD + +2 FAD+2 ADP+2 Pi  →  4 CO 2 +   6 NADH + 6H + +2 FADH 2  + 2 ATP

   

clipboard_ee9b67c8d71d2db1bc87c7e05120de851.png

Steps in the Citric Acid Cycle  

Step 1 . The first step is a condensation step, combining the two-carbon acetyl group (from acetyl CoA) with a four-carbon oxaloacetate molecule to form a six-carbon molecule of citrate. CoA is bound to a sulfhydryl group (-SH) and diffuses away to eventually combine with another acetyl group. This step is irreversible because it is highly exergonic. The rate of this reaction is controlled by negative feedback and the amount of ATP available. If ATP levels increase, the rate of this reaction decreases. If ATP is in short supply, the rate increases.

Step 2 . Citrate loses one water molecule and gains another as citrate is converted into its isomer, isocitrate.

Steps 3 and 4.  In step three, isocitrate is oxidized, producing a five-carbon molecule, α-ketoglutarate, together with a molecule of CO 2  and two electrons, which reduce NAD +  to NADH. This step is also regulated by negative feedback from ATP and NADH and by a positive effect of ADP. Steps three and four are both oxidation and decarboxylation steps, which release electrons that reduce NAD +  to NADH and release carboxyl groups that form CO 2  molecules. α-Ketoglutarate is the product of step three, and a succinyl group is the product of step four. CoA binds the succinyl group to form succinyl CoA. The enzyme that catalyzes step four is regulated by feedback inhibition of ATP, succinyl CoA, and NADH.

Step 5 . A phosphate group is substituted for coenzyme A, and a high- energy bond is formed. This energy is used in substrate-level phosphorylation (during the conversion of the succinyl group to succinate) to form either guanine triphosphate (GTP) or ATP. There are two forms of the enzyme, called isoenzymes, for this step, depending upon the type of animal tissue in which they are found. One form is found in tissues that use large amounts of ATP, such as heart and skeletal muscle. This form produces ATP. The second form of the enzyme is found in tissues that have a high number of anabolic pathways, such as liver. This form produces GTP. GTP is energetically equivalent to ATP; however, its use is more restricted. In particular, protein synthesis primarily uses GTP.

Step 6.  Step six is a dehydration process that converts succinate into fumarate with the help of an enzyme called succinate dehydrogenate . Two hydrogen atoms are transferred to FAD, producing FADH 2 . The energy contained in the electrons of these atoms is insufficient to reduce NAD +  but adequate to reduce FAD. Unlike NADH, this carrier remains attached to the enzyme and transfers the electrons to the electron transport chain directly. This process is made possible by the localization of the enzyme catalyzing this step inside the inner membrane of the mitochondrion.

Step 7 . Water is added to fumarate during step seven, and malate is produced. The last step in the citric acid cycle regenerates oxaloacetate by oxidizing malate. Another molecule of NADH is produced.

Products of the Citric Acid Cycle  

Two carbon atoms come into the citric acid cycle from each acetyl group, representing four out of the six carbons of one glucose molecule. Two carbon dioxide molecules are released on each turn of the cycle; however, these do not necessarily contain the most recently-added carbon atoms. The two acetyl carbon atoms will eventually be released on later turns of the cycle; thus, all six carbon atoms from the original glucose molecule are eventually incorporated into carbon dioxide. Each turn of the cycle forms three NADH molecules and one FADH 2  molecule. These carriers will connect with the last portion of aerobic respiration to produce ATP molecules. One GTP or ATP is also made in each cycle. Several of the intermediate compounds in the citric acid cycle can be used in synthesizing non-essential amino acids; therefore, the cycle is amphibolic (both catabolic and anabolic).

Summary  

In the citric acid cycle, the acetyl group from acetyl CoA is attached to a four-carbon oxaloacetate molecule to form a six-carbon citrate molecule. Through a series of steps, citrate is oxidized, releasing two carbon dioxide molecules for each acetyl group fed into the cycle. In the process, three NAD +  molecules are reduced to NADH, one FAD molecule is reduced to FADH 2 , and one ATP or GTP (depending on the cell type) is produced (by substrate-level phosphorylation). Because the final product of the citric acid cycle is also the first reactant, the cycle runs continuously in the presence of sufficient reactants.

U.S. flag

An official website of the United States government

The .gov means it's official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you're on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

  • Publications
  • Account settings
  • Browse Titles

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Physiology, krebs cycle.

Tamim O. Alabduladhem ; Bruno Bordoni .

Affiliations

Last Update: November 23, 2022 .

  • Introduction

The tricarboxylic acid (TCA) cycle, also known as the Krebs cycle or citric acid cycle, is an important cell's metabolic hub. It is composed of eight enzymes, all of which are within the mitochondrial matrix except the outlier succinate dehydrogenase, which is related to the respiratory chain on the inner mitochondrial membrane. The cycle serves as a gateway for aerobic metabolism for molecules that can convert to an acetyl group or dicarboxylic acid. Regulation of the TCA cycle occurs at three distinct points that include the three following enzymes: citrate synthase, isocitrate dehydrogenase, and alpha-ketoglutarate dehydrogenase. The cycle also plays a role in replenishing precursors for the storage form of fuels such as amino acids and cholesterol. [1]

  • Issues of Concern

The Krebs cycle, by itself, does not require the presence of oxygen; this element is necessary for the last stage of aerobic cellular respiration, i.e., oxidative phosphorylation.

Organic molecules endowed with energy (carbohydrates, lipids, proteins) are split in previous reactions. Before entering the Krebs cycle, they transform into acetyl-CoA, a molecule formed by an acetyl group (CH3CO-) and by an acyl transporter called coenzyme A.

However, the preferred source of acetyl-CoA remains glycolysis. The acetyl group is then oxidized, and the energy obtained is used for the synthesis of ATP in cooperation with oxidative phosphorylation. In eukaryotes, the Krebs cycle reactions take place in the mitochondrial matrix, a dense solution that surrounds the mitochondria crests: in addition to water, the matrix contains all the enzymes necessary for the biochemical reactions of the cycle, coenzymes, and phosphates.The Krebs cycle is controlled and regulated by the availability of the NAD+ and FAD substrates, while high concentrations of NADH inhibit it.

  • Cellular Level

Glucose metabolism takes place in the cytosol without the need for oxygen by a process termed glycolysis. It yields a small amount of ATP, and the three-carbon compound pyruvate. After the transportation of pyruvate into the mitochondria, pyruvate dehydrogenase complex (PDC) facilitates the conversion of pyruvate to acetyl-CoA and CO2. Each molecule of acetyl-CoA entering the TCA cycle yields 12 ATP molecules. The (PDC) has three protein subunits and requires five cofactors for its enzymatic function. The requirement of cofactors ensures the ability of the complex to be regulated. In high blood sugar levels, most acetyl-CoA will be derived from glucose, more specifically, pyruvate. However, in starvation or fasting states, beta-oxidation contributes to the production of acetyl-CoA. Acetyl-CoA undergoes oxidation to CO2 in eight steps, and the energy produced from these reactions is stored in NADH+H+, FADH2, and GTP. NADH+H+ and FADH2 then oxidize in the electron transport chain (mitochondrial respiratory chain), terminating in ATP synthesis. [2]

Intermediated from the TCA cycle are precursors for both catabolic and anabolic processes. It connects several metabolic processes (e.g., glycolysis, gluconeogenesis, ketogenesis, lipogenesis). [3]

These three mechanisms regulate the activity of pyruvate dehydrogenase complex (PDC): covalent modification being the primary form of regulation, allosteric regulation, and transcriptional regulation. The covalent modification takes place when the first subunit of the PDC, pyruvate decarboxylase, is phosphorylated. This phosphorylation results in decreased PDC activity and an increase of ADP or pyruvate (signaling the requirement for more acetyl-CoA in the TCA cycle, which downregulates PDC). Calcium ions upregulate phosphatase’s activity; phosphatase, in turn, dephosphorylates PDC rendering it active. Allosteric regulation of PDC entails the direct mechanism of substrate activation or product inhibition. For instance, when there is an excess release of Acetyl-CoA from E2 or NADH from E3, these products act to inhibit PDC directly. In contrast, an increase in the levels of CoASH (precursor to acetyl-CoA) or NAD+ will directly activate PDC. The last type of regulation of PDC activity is transcriptional regulation, which is dependent on the number of enzymes produced in fasting and fed conditions. In the fed state, enzyme production increases due to the effect of insulin, but it reduces in fasting states. [4]

  • Development

The Krebs cycle is also crucial during development. To make an example, the energy obtained from this metabolic pathway is essential for the adequate growth of the endothelial system, which will guide the formation of the blood and lymphatic vessels.

If the different phases of the Krebs cycle are not present in the fetal period, the baby's heart may have problems at birth. The alteration of the cycle causes an increase in cortisol, which alters the metabolism of the placenta and fetal development, including the correct function of the heart of the future child. These alterations can lead to death.

  • Organ Systems Involved

The Krebs cycle is present in every cell that uses oxygen to produce energy. This metabolic pathway is used as an anabolic cellular principle but also in the presence of catabolism.

Citrate Synthesis

The enzyme citrate synthase catalyzes the formation of citrate from acetyl CoA and oxaloacetate, often regarded as the first step of the TCA cycle. This reaction is virtually irreversible and has a delta-G-prime of -7.7 Kcal/M that strongly favors citrate formation. The availability of substrates and products regulates the activity of citrate synthase. For instance, citrate itself acts as an inhibitor for citrate synthase, while oxaloacetate’s binding to it increases its affinity for acetyl-CoA. It bears mention that phosphofructokinase-1 in glycolysis is inhibited by citrate, while it activates acetyl-CoA carboxylase for fatty acid synthesis. This point illustrates the interconnectivity of our metabolic cycles. [5]

Isomerization of Citrate

The reversible conversion of citrate to isocitrate is catalyzed by the enzyme aconitase, which contains an iron-sulfur center that facilitates the hydroxyl group migration. Cis-aconitate is the intermediate product of this reaction. [6]

Oxidative Decarboxylation of Isocitrate

The oxidative decarboxylation of isocitrate to alpha-ketoglutarate becomes catalyzed by NAD+ -dependent isocitrate dehydrogenase producing CO2, NADH, and a proton; this is the rate-limiting step of the TCA cycle. Production of the first reduced coenzyme in the cycle takes place at this reaction. The tendency of this reaction to produce gas makes it irreversible. ADP and calcium ions allosterically regulate isocitrate dehydrogenase by activating it, while ATP and NADH inhibit its activity. [7]

Oxidative Decarboxylation of Alpha-ketoglutarate

The conversion of alpha-ketoglutarate to succinyl-CoA is catalyzed by the alpha-ketoglutarate dehydrogenase complex producing NADH, CO2, and H+. The function of the alpha-ketoglutarate dehydrogenase complex is analogous to PDC. Alpha-ketoglutarate becomes decarboxylated by E1 of this complex, transferring the four remaining carbons to thiamine pyrophosphate. Thiamine pyrophosphate is the first cofactor. Then the succinyl group transfers to CoASH by E2 with the help of FAD. The final step involves the resynthesis of FAD along with NADH from NAD+ by E3. This last step ensures the maintenance of substrates and cofactors required to continue the dehydrogenase complex activity. The cofactors necessary for alpha-ketoglutarate dehydrogenase complex include thiamine pyrophosphate, lipoic acid, coenzyme A, NAD+, and FAD. Succinyl-CoA, NADH, and ATP inhibit the alpha-ketoglutarate dehydrogenase complex. [8] [9]

Cleavage of Succinyl Coenzyme A

The enzyme succinate thiokinase catalyzes the reversible interconversion of succinyl-CoA to succinate by cleaving succinyl CoA’s thioester bond. The enzyme uses inorganic phosphate and dinucleotide to produce trinucleotide and CoA. This coupled reaction is called substrate-level phosphorylation, just like what happens in glycolysis. [10]

Oxidation of Succinate

Succinate dehydrogenase is also called complex II   due to its role in the aerobic respiration chain. It catalyzes the reduction of ubiquinone to ubiquinol. The TCA cycle catalyzes the oxidation of succinate to fumarate, producing a reduced FADH2 from FAD. [11]

Hydration of Fumarate

The reversible hydration of fumarate to malate is catalyzed by fumarase (or fumarate hydratase). In another attempt to illustrate the interconnectedness of metabolic pathways, note that fumarate production also occurs in the urea cycle. [12]

Oxidation of Malate

Malate dehydrogenase is the catalyst in the reversible oxidation of malate to oxaloacetate, which is the last step of the TCA cycle. This enzyme plays a crucial role in NADH oxidation within the TCA cycle. The delta-G-prime is positive, which indicates that the reaction favors malate. However, the consumption of oxaloacetate by citrate synthase drives this reaction forward to produce more oxaloacetate. [13]

Cataplerotic Processes

Citric acid intermediates can leave the cycle to participate in the biosynthesis of other compounds. Citrate can be directed toward fatty acids; succinyl-CoA to heme synthesis; alpha-ketoglutarate to amino acid synthesis, purine synthesis, and neurotransmitter synthesis; oxaloacetate to amino acid synthesis, and malate to gluconeogenesis. [14] [4]

Anaplerotic Processes

Intermediates are inserted into the TCA cycle to replace the cataplerotic processes and ensure the continuation of the cycle. For instance, pyruvate can enter the cycle throughout the body through pyruvate carboxylase, which inserts additional oxaloacetate into the cycle. This process causes the reaction to be pushed forward toward the already exergonic citrate synthase, as there is more oxaloacetate to participate in the reaction. The liver is another example, as it can produce alpha-ketoglutarate by oxidative deamination or transamination of glutamate. [15] [4]

  • Related Testing

Evaluating mitochondrial function involves evaluating the Krebs cycle. For example, in nonalcoholic liver disease (NAFLD), there is a mitochondrial malfunction, and it is one of the diagnostic cornerstones. Some authors suggest comparing the plasma values of isocitrate and citrate for a finding of mitochondrial alteration.

The search for plasma values of mitochondrial metabolites can be used to understand how mitochondria are working.

  • Pathophysiology

Mitochondrial dysfunction can result from an excess of calories introduced through food; the Krebs cycle can no longer find a balance between the molecules to be degraded and the number of molecules available. Obesity shows a mitochondrial alteration, with an increase in oxidative stress and the production of reactive oxygen species, inflammation, and apoptosis.

Mitochondrial dysfunction can also mean overwork compared to normal values. In Duchenne pathology (in an animal model), an increase of mitochondrial metabolites is present in different tissues, such as the diaphragm and peripheral muscles, the central nervous system. The reasons are probably related to oxidative stress.

  • Clinical Significance

Pyruvate Dehydrogenase Complex Deficiency

Pyruvate dehydrogenase complex deficiency is a neurodegenerative disorder due to an abnormal pyruvate decarboxylase subunit caused by a mutated X-linked PDHAD gene. This mutation leads to the impaired conversion of pyruvate to acetyl-CoA. Since there is an excess accumulation of pyruvate, lactate dehydrogenase will convert it to lactate leading to potentially fatal metabolic acidosis. Other symptoms include neonatal-onset lethargy, hypotonicity, muscle spasticity, neurodegeneration, and early death. [16] [17] [18]

Leigh Syndrome

Subacute necrotizing encephalomyelopathy or Leigh syndrome is a progressive neurological disorder due to gene mutations encoding proteins of the PDC. In most children, the first observed sign is the inability to perform motor skills previously acquired. Other symptoms include loss of head control, poor suckling, recurrent vomiting, and loss of appetite. [19] [20] [21]

Thiamine Deficiency

Thiamine deficiency is similar to pyruvate dehydrogenase complex deficiency in that it will lead to the shunting of pyruvate to lactate leading to metabolic acidosis. However, the culprit here is a deficiency in the active form of thiamine (thiamine pyrophosphate) rather than PDC. Acute thiamine deficiency is dry beriberi, while chronic thiamine deficiency is wet beriberi. Dry beriberi characteristically demonstrates diminished reflexes and symmetric peripheral neuropathy with motor and sensory changes. On the other hand, wet beriberi classically affects the heart leading to tachycardia, dilated cardiomyopathy, high-output congestive heart failure, and peripheral edema. [22] [23]

Fumarase Deficiency

Fumarase deficiency is a rare autosomal recessive metabolic disorder of the TCA cycle due to a mutation in the FH gene. It is characterized by a deficiency of the enzyme fumarase hydrates, which leads to the buildup of fumaric acid. It is a condition that mainly affects the nervous system. Affected children may have severe developmental delay, microcephaly, hypotonia, encephalopathy, seizures, psychomotor retardation, and failure to thrive. [24] [25] [26] [27]

Mutations of Isocitrate Dehydrogenase

Researchers have found mutations of isocitrate dehydrogenase in several types of cancers, including leukemia, gliomas, and sarcomas. IDH mutations can be useful for the differential diagnosis and subclassification of human gliomas. The normal function of IDH is to catalyze the oxidative decarboxylation of isocitrate to alpha-ketoglutarate. Mutant IDH catalyzes the formation of 2-hydroxyglutarate instead of alpha-ketoglutarate. 2-hydroxyglutarate is an oncometabolite that causes DNA and histone hypermethylation leading to neoplasia. 2-hydroxyglutarate can be used as a biomarker for cancer in patients with inborn errors of metabolism. [28] [29] [7] [30]

  • Review Questions
  • Access free multiple choice questions on this topic.
  • Comment on this article.

Krebs cycle Contributed by Katherine Humphries

Disclosure: Tamim Alabduladhem declares no relevant financial relationships with ineligible companies.

Disclosure: Bruno Bordoni declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

  • Cite this Page Alabduladhem TO, Bordoni B. Physiology, Krebs Cycle. [Updated 2022 Nov 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

In this Page

Bulk download.

  • Bulk download StatPearls data from FTP

Related information

  • PMC PubMed Central citations
  • PubMed Links to PubMed

Similar articles in PubMed

  • The tricarboxylic acid cycle in L₃ Teladorsagia circumcincta: metabolism of acetyl CoA to succinyl CoA. [Exp Parasitol. 2011] The tricarboxylic acid cycle in L₃ Teladorsagia circumcincta: metabolism of acetyl CoA to succinyl CoA. Simcock DC, Walker LR, Pedley KC, Simpson HV, Brown S. Exp Parasitol. 2011 May; 128(1):68-75. Epub 2011 Feb 12.
  • Global transcription analysis of Krebs tricarboxylic acid cycle mutants reveals an alternating pattern of gene expression and effects on hypoxic and oxidative genes. [Mol Biol Cell. 2003] Global transcription analysis of Krebs tricarboxylic acid cycle mutants reveals an alternating pattern of gene expression and effects on hypoxic and oxidative genes. McCammon MT, Epstein CB, Przybyla-Zawislak B, McAlister-Henn L, Butow RA. Mol Biol Cell. 2003 Mar; 14(3):958-72.
  • Tricarboxylic acid cycle enzyme activities in a mouse model of methylmalonic aciduria. [Mol Genet Metab. 2019] Tricarboxylic acid cycle enzyme activities in a mouse model of methylmalonic aciduria. Wongkittichote P, Cunningham G, Summar ML, Pumbo E, Forny P, Baumgartner MR, Chapman KA. Mol Genet Metab. 2019 Dec; 128(4):444-451. Epub 2019 Oct 17.
  • Review The α-ketoglutarate dehydrogenase complex in cancer metabolic plasticity. [Cancer Metab. 2017] Review The α-ketoglutarate dehydrogenase complex in cancer metabolic plasticity. Vatrinet R, Leone G, De Luise M, Girolimetti G, Vidone M, Gasparre G, Porcelli AM. Cancer Metab. 2017; 5:3. Epub 2017 Feb 2.
  • Review Mitochondrial dysfunctions in cancer: genetic defects and oncogenic signaling impinging on TCA cycle activity. [Cancer Lett. 2015] Review Mitochondrial dysfunctions in cancer: genetic defects and oncogenic signaling impinging on TCA cycle activity. Desideri E, Vegliante R, Ciriolo MR. Cancer Lett. 2015 Jan 28; 356(2 Pt A):217-23. Epub 2014 Mar 12.

Recent Activity

  • Physiology, Krebs Cycle - StatPearls Physiology, Krebs Cycle - StatPearls

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

Connect with NLM

National Library of Medicine 8600 Rockville Pike Bethesda, MD 20894

Web Policies FOIA HHS Vulnerability Disclosure

Help Accessibility Careers

statistics

Library homepage

  • school Campus Bookshelves
  • menu_book Bookshelves
  • perm_media Learning Objects
  • login Login
  • how_to_reg Request Instructor Account
  • hub Instructor Commons
  • Download Page (PDF)
  • Download Full Book (PDF)
  • Periodic Table
  • Physics Constants
  • Scientific Calculator
  • Reference & Cite
  • Tools expand_more
  • Readability

selected template will load here

This action is not available.

Biology LibreTexts

6.6: The Krebs/TCA/Citric acid cycle

  • Last updated
  • Save as PDF
  • Page ID 16448

  • Gerald Bergtrom
  • University of Wisconsin-Milwaukee

Glycolysis through fermentative reactions produces ATP anaerobically. The evolution of respiration (the aerobic use of oxygen to efficiently burn nutrient fuels) had to wait until photosynthesis created the oxygenic atmosphere we live in now. Read more about the source of our oxygenic atmosphere in Dismukes GC et al. [(2001) The origin of atmospheric oxygen on earth: the innovation of oxygenic photosynthesis. Proc. Nat. Acad. Sci. USA 98:2170-2175].

The Krebs cycle is the first pathway of oxygenic respiration. Evolution of this respiration and the chemical bridge from glycolysis to the Krebs cycle, no doubt occurred a few reactions at a time, perhaps at first as a means of protecting anaerobic cells from the ‘poisonous’ effects of oxygen. Later, natural selection fleshed out the aerobic Krebs cycle, electron transport and oxidative phosphorylation pathways we see today.

Whatever its initial utility, these reactions were an adaptive response to the increase in oxygen in the earth’s atmosphere. As a pathway for getting energy out of nutrients, respiration is much more efficient than glycolysis. Animals rely on it, but even plants and photosynthetic algae use the respiratory pathway when sunlight is not available! Here we focus on oxidative reactions in mitochondria, beginning with pyruvate oxidation and continuing to the redox reactions of the Krebs cycle.

After entering the mitochondria, pyruvate dehydrogenase catalyzes pyruvate oxidation to Acetyl-S-Coenzyme A ( Ac-S-CoA ). Then the Krebs cycle completely oxidizes the Ac-S- CoA . These mitochondrial redox reactions generate CO2 and lot of reduced electron carriers (NADH, FADH2). The free energy released in these redox reactions is coupled to the synthesis of only one ATP per pyruvate oxidized (i.e., two per the glucose we started with!). It is the NADH and FADH2 molecules have captured most of the free energy in the original glucose molecules. These entry of pyruvate into the mitochondrion and its oxidation are summarized below.

clipboard_e8f55c1a2f07cc12e34b1fa27a888d591.png

Pyruvate oxidation converts a 3C carbohydrate into acetate, a 2C molecule, releasing a molecule of CO2. In this highly exergonic reaction, CoA-SH forms a high-energy thioester linkage with the acetate in Ac-S-CoA. The oxidation of pyruvic acid results in the reduction of NAD+, production of Ac-S-CoA and a molecule of CO2, as shown below.

clipboard_e79a21a3c2882ff9080dda30f2ab4dab4.png

The Krebs cycle functions during respiration to oxidize Ac-S-CoA and to reduce NAD+ and FAD to NADH and FADH2 (respectively). Intermediates of the Krebs cycle also function in amino acid metabolism and interconversions. All aerobic organisms alive today share the Krebs cycle we see in humans. This is consistent with its spread early in the evolution of our oxygen environment. Because of the central role of Krebs cycle intermediates in other biochemical pathways, parts of the pathway may even have pre- dated the complete respiratory pathway. The Krebs cycle takes place in mitochondria of eukaryotic cells.

After the oxidation of pyruvate, the Ac-S-CoA enters the Krebs cycle, condensing with oxaloacetate in the cycle to form citrate . There are four redox reactions in the Krebs cycle. As we discuss the Krebs cycle, look for the accumulation of reduced electron carriers (FADH2, NADH) and a small amount of ATP synthesis by substrate-level phosphorylation. Also, follow the carbons in pyruvate into CO2. The Krebs Cycle as it occurs in animals is summarized below.

clipboard_edcefdfe8543c2834f441715dd29d7775.png

To help you understand the events of the cycle,

1. find the two molecules of CO2 produced in the Krebs cycle itself.

2. find GTP (which quickly transfers its phosphate to ADP to make ATP). Note that in bacteria, ATP is made directly at this step.

3. count all of the reduced electron carriers (NADH, FADH2). Both of these electron carriers carry a pair of electrons. If you include the electrons on each of the NADH molecules made in glycolysis, how many electrons have been removed from glucose during its complete oxidation?

Remember that glycolysis produces two pyruvates per glucose, and thus two molecules of Ac-S-CoA. Thus, the Krebs cycle turns twice for each glucose entering the glycolytic pathway. The high-energy thioester bonds formed in the Krebs cycle fuel ATP synthesis as well as the condensation of oxaloacetate and acetate to form citrate in the first reaction. Each NADH carries about 50 Kcal of the 687 Kcal of free energy originally available in a mole of glucose; each FADH2 carries about 45 Kcal of this free energy. This energy will fuel ATP production during electron transport and oxidative phosphorylation.

159 Highlights of the Krebs Cycle

Finally, the story of the discovery of the Krebs cycle is as interesting as the cycle itself! Albert Szent-Györgyi won a Nobel Prize in 1937 for discovering some organic acid oxidation reactions initially thought to be part of a linear pathway. Hans Krebs did the elegant experiments showing that the reactions were part of a cyclic pathway. He proposed (correctly!) that the cycle would be a supercatalyst that would catalyze the oxidation of yet another organic acid. Some of the experiments are described by Krebs and his coworkers in their classic paper: Krebs HA, et al. [(1938) The formation of citric and α-ketoglutaric acids in the mammalian body. Biochem. J. 32: 113–117]. Hans Krebs and Fritz Lipmann shared the 1953 Nobel Prize in Physiology or Medicine. Krebs was recognized for his elucidation of the TCA cycle, which now more commonly carries his name. Lipmann was recognized for proposing ATP as the mediator between food (nutrient) energy and intracellular work energy, and for discovering the reactions that oxidize pyruvate and synthesize Ac-S-CoA, bridging the Krebs Cycle and oxidative phosphorylation (to be considered iin the next chapter).

160 Discovery of the Krebs Cycle

You can read Krebs’ review of his own research in Krebs HA [(1970) The history of the tricarboxylic acid cycle . Perspect. Biol. Med. 14:154-170]. For a classic read on how Krebs described his supercatalyst suggestion, click Hans Krebs Autobiographical Comments. For more about the life of Lipmann, check out the brief Nobel note on the Fritz Lipmann Biography .

assignment on krebs cycle

  • DNA Replication
  • Active Transport
  • Cellular Receptors
  • Endocytosis and Exocytosis
  • Enzyme Inhibition
  • Enzyme Kinetics
  • Protein Structure
  • Transcription of DNA
  • Translation of DNA
  • Anaerobic Respiration
  • Electron Transport Chain
  • Gluconeogenesis
  • Calcium Regulation
  • External Balance of Potassium
  • Internal Balance of Potassium
  • Sodium Regulation
  • Cell Membrane
  • Endoplasmic Reticulum
  • Golgi Apparatus
  • Mitochondria
  • Blood Vessels
  • Cellular Adaptations
  • Epithelial Cells
  • Muscle Histology
  • Structure of Glands
  • Control of Stroke Volume
  • Control of Heart Rate
  • Cardiac Cycle
  • Cardiac Pacemaker Cells
  • Conduction System
  • Contraction of Cardiac Muscle
  • Ventricular Action Potentials
  • Blood Flow in Vessels
  • Control of Blood Pressure
  • Capillary Exchange
  • Flow In Peripheral Circulation
  • Venous Return
  • Cardiac Muscle
  • Hepatic Circulation
  • Skeletal Muscle
  • Airway Resistance
  • Lung Volumes
  • Mechanics of Breathing
  • Gas Exchange
  • Oxygen Transport in The Blood
  • Transport of Carbon Dioxide in the Blood
  • Ventilation-Perfusion Matching
  • Chemoreceptors
  • Cough Reflex
  • Neural Control of Ventilation
  • Respiratory Regulation of Acid-Base Balance
  • Responses of The Respiratory System to Stress
  • Regulation of Saliva
  • Secretion of Saliva
  • Gastric Acid Production
  • Gastric Mucus Production
  • Digestion and Absorption
  • Histology and Cellular Function of the Small Intestine
  • Absorption in the Large Intestine
  • Large Intestinal Motility
  • Bilirubin Metabolism
  • Carbohydrate Metabolism in the Liver
  • Lipid Metabolism in the Liver
  • Protein and Ammonia Metabolism in the Liver
  • Storage Functions of the Liver
  • Bile Production
  • Function of The Spleen
  • Exocrine Pancreas
  • Somatostatin
  • Proximal Convoluted Tubule
  • Loop of Henle
  • Distal Convoluted Tubule and Collecting Duct
  • Storage Phase of Micturition
  • Voiding Phase of Micturition
  • Antidiuretic Hormone
  • Renin-Angiotensin-Aldosterone System
  • Urinary Regulation of Acid-Base Balance
  • Water Filtration and Reabsorption
  • Development of the Reproductive System
  • Gametogenesis
  • Gonadotropins and the Hypothalamic Pituitary Axis
  • Menstrual Cycle
  • Placental Development
  • Fetal Circulation
  • Maternal Adaptations in Pregnancy
  • Cells of the Nervous System
  • Central Nervous System
  • Cerebrospinal Fluid
  • Neurotransmitters
  • Peripheral Nervous System
  • Action Potential
  • Excitatory and Inhibitory Synaptic Signalling
  • Resting Membrane Potential
  • Synaptic Plasticity
  • Synaptic Transmission
  • Ascending Tracts
  • Auditory Pathway
  • Consciousness and Sleep
  • Modalities of Sensation
  • Pain Pathways
  • Sensory Acuity
  • Visual Pathway
  • Descending Tracts
  • Lower Motor Neurones
  • Muscle Stretch Reflex
  • Upper Motor Neurones
  • Aqueous Humour
  • Ocular Accommodation
  • Thyroid Gland
  • Parathyroid Glands
  • Adrenal Medulla
  • Zona Glomerulosa
  • Zona Fasciculata
  • Zona Reticularis
  • Endocrine Pancreas
  • The Hypothalamus
  • Anterior Pituitary
  • Posterior Pituitary
  • White Blood Cells – Summary
  • Barriers to Infection
  • Infection Recognition Molecules
  • Phagocytosis
  • The Complement System
  • Antigen Processing and Presentation
  • Primary and Secondary Immune Responses
  • T Cell Memory
  • Acute Inflammation
  • Autoimmunity
  • Chronic Inflammation
  • Hypersensitivity Reactions
  • Immunodeficiency
  • Types of Immunity
  • Antibiotics
  • Viral Infection
  • Blood Groups
  • Coagulation
  • Erythropoiesis
  • Iron Metabolism
  • Mononuclear Phagocyte System

Original Author(s): Aarushi Khanna Last updated: 13th March 2023 Revisions: 15

  • 1 Link Reaction
  • 2.1 Net Output
  • 3 Regulation of the TCA Cycle
  • 4 Clinical Relevance – Defects of the TCA Cycle

In order for ATP to be produced through oxidative phosphorylation , electrons are required. This allows ATP to pass down the electron transport chain . These electrons come from electron carriers such as NADH and FADH₂, which are produced by the Tricarboxylic Acid Cycle (TCA cycle, also known as the Kreb’s/Citric Acid cycle).

In this article, we will outline the steps and regulation of this essential part of cellular physiology.

Link Reaction

Prior to the TCA cycle, glycolysis has occurred, which generates molecules including pyruvate, ATP, and NADH. Pyruvate is then decarboxylated  to form acetyl-coA by the pyruvate decarboxylase complex . Acetyl-CoA is the intermediate that then enters the TCA cycle.

The TCA Cycle

The TCA cycle is a central pathway that provides a unifying point for many metabolites, which feed into it at various points. It takes place over eight different steps:

  • Step 1:   Acetyl CoA (two-carbon molecule) joins with oxaloacetate (four-carbon molecule) to form citrate (six-carbon molecule).
  • Step 2: Citrate is converted to isocitrate (an isomer of citrate)
  • Step 3: Isocitrate is oxidised to alpha-ketoglutarate (a five-carbon molecule) which results in the release of carbon dioxide . One NADH molecule is formed.

The enzyme responsible for catalysing this step is  isocitrate dehydrogenase. This is a rate-limiting step, as isocitrate dehydrogenase is an allosterically controlled enzyme .

  • Step 4: Alpha-ketoglutarate is oxidised to form a four-carbon molecule. This binds to coenzyme A, forming succinyl CoA. A second molecule of NADH is produced, alongside a second molecule of carbon dioxide .
  • Step 5: Succinyl CoA is then converted to succinate (four-carbon molecule) and one GTP molecule is produced.
  • Step 6: Succinate is converted into fumarate (four-carbon molecule) and a molecule of FADH₂ is produced.
  • Step 7: Fumarate is converted to malate (another four-carbon molecule).
  • Step 8: Malate is then converted into oxaloacetate. The third molecule of NADH is also produced.

Fig 1 – Diagram showing the steps of the TCA cycle.

While the primary role of the TCA cycle is the production of NADH and FADH₂, it also produces molecules that supply various biosynthetic processes. These enter or exit the cycle at various points depending on demand. For example, alpha-ketoglutarate can leave the cycle to be converted into amino acids, and succinate  can be converted to haem.

Each cycle produces:

  • Two molecules of carbon dioxide .
  • Three molecules of NADH .
  • Three hydrogen ions ( H+ ).
  • One molecule of FADH₂
  • One molecule of GTP .

Each molecule of glucose produces two molecules of pyruvate, which in turn produces two molecules of acetyl-CoA. Therefore, each molecule of glucose produces double the net output of each cycle .

Regulation of the TCA Cycle

This process is regulated in a variety of ways:

  • Metabolites: Products of the cycle provide negative feedback on the enzymes that catalyse it. For example, NADH inhibits the majority of the enzymes found in the cycle.
  • Citrate: Inhibits phosphofructokinase, a key enzyme in glycolysis. This reduces the rate of production of pyruvate and therefore of acetyl-CoA.
  • Calcium:  Accelerates the TCA cycle by stimulating the link reaction.

Clinical Relevance – Defects of the TCA Cycle

There are in fact no known defects of the TCA cycle that are compatible with life. This highlights the importance of this step in ATP production for sustaining life.

In order for ATP to be produced through oxidative phosphorylation , electrons are required. This allows ATP to pass down the electron transport chain . These electrons come from electron carriers such as NADH and FADH₂, which are produced by the Tricarboxylic Acid Cycle (TCA cycle, also known as the Kreb's/Citric Acid cycle).

[start-clinical]

Clinical Relevance - Defects of the TCA Cycle

[end-clinical]

Found an error? Is our article missing some key information? Make the changes yourself here!

Once you've finished editing, click 'Submit for Review', and your changes will be reviewed by our team before publishing on the site.

We use cookies to improve your experience on our site and to show you relevant advertising. To find out more, read our privacy policy .

Privacy Overview

Sciencing_Icons_Science SCIENCE

Sciencing_icons_biology biology, sciencing_icons_cells cells, sciencing_icons_molecular molecular, sciencing_icons_microorganisms microorganisms, sciencing_icons_genetics genetics, sciencing_icons_human body human body, sciencing_icons_ecology ecology, sciencing_icons_chemistry chemistry, sciencing_icons_atomic & molecular structure atomic & molecular structure, sciencing_icons_bonds bonds, sciencing_icons_reactions reactions, sciencing_icons_stoichiometry stoichiometry, sciencing_icons_solutions solutions, sciencing_icons_acids & bases acids & bases, sciencing_icons_thermodynamics thermodynamics, sciencing_icons_organic chemistry organic chemistry, sciencing_icons_physics physics, sciencing_icons_fundamentals-physics fundamentals, sciencing_icons_electronics electronics, sciencing_icons_waves waves, sciencing_icons_energy energy, sciencing_icons_fluid fluid, sciencing_icons_astronomy astronomy, sciencing_icons_geology geology, sciencing_icons_fundamentals-geology fundamentals, sciencing_icons_minerals & rocks minerals & rocks, sciencing_icons_earth scructure earth structure, sciencing_icons_fossils fossils, sciencing_icons_natural disasters natural disasters, sciencing_icons_nature nature, sciencing_icons_ecosystems ecosystems, sciencing_icons_environment environment, sciencing_icons_insects insects, sciencing_icons_plants & mushrooms plants & mushrooms, sciencing_icons_animals animals, sciencing_icons_math math, sciencing_icons_arithmetic arithmetic, sciencing_icons_addition & subtraction addition & subtraction, sciencing_icons_multiplication & division multiplication & division, sciencing_icons_decimals decimals, sciencing_icons_fractions fractions, sciencing_icons_conversions conversions, sciencing_icons_algebra algebra, sciencing_icons_working with units working with units, sciencing_icons_equations & expressions equations & expressions, sciencing_icons_ratios & proportions ratios & proportions, sciencing_icons_inequalities inequalities, sciencing_icons_exponents & logarithms exponents & logarithms, sciencing_icons_factorization factorization, sciencing_icons_functions functions, sciencing_icons_linear equations linear equations, sciencing_icons_graphs graphs, sciencing_icons_quadratics quadratics, sciencing_icons_polynomials polynomials, sciencing_icons_geometry geometry, sciencing_icons_fundamentals-geometry fundamentals, sciencing_icons_cartesian cartesian, sciencing_icons_circles circles, sciencing_icons_solids solids, sciencing_icons_trigonometry trigonometry, sciencing_icons_probability-statistics probability & statistics, sciencing_icons_mean-median-mode mean/median/mode, sciencing_icons_independent-dependent variables independent/dependent variables, sciencing_icons_deviation deviation, sciencing_icons_correlation correlation, sciencing_icons_sampling sampling, sciencing_icons_distributions distributions, sciencing_icons_probability probability, sciencing_icons_calculus calculus, sciencing_icons_differentiation-integration differentiation/integration, sciencing_icons_application application, sciencing_icons_projects projects, sciencing_icons_news news.

  • Share Tweet Email Print
  • Home ⋅
  • Science ⋅
  • Biology ⋅
  • Cell (Biology): An Overview of Prokaryotic & Eukaryotic Cells

The Krebs Cycle Made Easy

assignment on krebs cycle

Which Molecules Enter & Leave the Krebs Cycle?

The Krebs cycle, named after 1953 Nobel Prize winner and physiologist Hans Krebs, is a series of metabolic reactions that take place in the mitochondria of eukaryotic cells . Put more simply, this means that bacteria do not have the cellular machinery for the Krebs cycle, so it limited to plants, animals and fungi.

Glucose is the molecule that is ultimately metabolized by living things to derive energy, in the form of adenosine triphosphate, or ATP . Glucose can be stored in the body in numerous forms; glycogen is little more than a long chain of glucose molecules that is stored in muscle and liver cells, while dietary carbohydrates, proteins and fats have components that can be metabolized to glucose as well. When a molecule of glucose enters a cell, it is broken down in the cytoplasm into pyruvate.

What happens next depends on whether the pyruvate enters the aerobic respiration path (the usual result) or the lactate fermentation path (used in bouts of high-intensity exercise or oxygen deprivation) before it ultimately allows for ATP production and the release of carbon dioxide (CO 2 ) and water (H 2 O) as by-products.

The Krebs cycle – also called the citric acid cycle or the tricarboxylic acid (TCA) cycle – is the first step in the aerobic pathway, and it operates to continually synthesize enough of a substance called oxaloacetate to keep the cycle going, although, as you'll see, this is not really the cycle's "mission." The Krebs cycle supplies other benefits as well. Because it includes some eight reactions (and, correspondingly, nine enzymes) involving nine distinct molecules, it is helpful to develop tools to keep the important points of the cycle straight in your mind.

Glycolysis: Setting the Stage

Glucose is a six-carbon (hexose) sugar that in nature is usually in the form of a ring. Like all monosaccharides (sugar monomers), it consists of carbon, hydrogen and oxygen in a 1-2-1 ratio, with a formula of C 6 H 12 O 6 . It is one of the end products of protein, carbohydrate and fatty-acid metabolism and serves as fuel in every type of organism from single-celled bacteria to human beings and larger animals.

Glycolysis is anaerobic in the strict sense of "without oxygen." That is, the reactions proceed whether O 2 is present in cells or not. Be careful to distinguish this from "oxygen must not be present," although this is the case with some bacteria that are actually killed by oxygen and are known as obligate anaerobes.

In the reactions of glycolysis, the six-carbon glucose is initially phosphorylated – that is, it has a phosphate group appended to it. The resulting molecule is a phosphorylated form of fructose (fruit sugar). This molecule is then phosphorylated a second time. Each of these phosphorylations requires a molecule of ATP, both of which are converted to adenosine diphosphate, or ADP. The six-carbon molecule is then converted into two three-carbon molecules, which are quickly converted to pyruvate. Along the way, in the processing of both molecules, 4 ATP are produced with the help of two molecules of NAD+ (nicotinamide adenine dinucleotide) that are converted to two molecules of NADH. Thus for every glucose molecule that enters glycolysis, a net of two ATP, two pyruvate and two NADH are produced, while two NAD+ are consumed .

The Krebs Cycle: Capsule Summary

As noted previously, the fate of pyruvate depends on the metabolic demands and the environment of the organism in question. In prokaryotes, glycolysis plus fermentation provides almost all of the single cell's energy needs, although some of these organisms have evolved electron transport chains that allow them to make use of oxygen to liberate ATP from metabolites (products) of glycolysis . In prokaryotes as well as in all eukaryotes but yeast, if there is no oxygen available or if the cell's energy needs cannot be fully met through aerobic respiration, pyruvate is converted to lactic acid via fermentation under the influence of the enzyme lactate dehydrogenase, or LDH.

Pyruvate destined for the Krebs cycle moves from the cytoplasm across the membrane of cell organelles (functional components in the cytoplasm) called mitochondria . Once in the mitochondrial matrix, which is a sort of cytoplasm for the mitochondria themselves, it is converted under the influence of the enzyme pyruvate dehydrogenase to a different three-carbon compound called acetyl coenzyme A or acetyl CoA . Many enzymes can be picked out from a chemical line-up because of the "-ase" suffix they share.

At this point you should avail yourself of a diagram detailing the Krebs cycle, as it is the only way to meaningfully follow along; see the Resources for an example.

The reason the Krebs cycle is named as such is that one of its main products, oxaloacetate, is also a reactant. That is, when the two-carbon acetyl CoA created from pyruvate enters the cycle from "upstream," it reacts with oxaloacetate, a four-carbon molecule, and forms citrate, a six-carbon molecule. Citrate, a symmetrical molecule, includes three carboxyl groups , which have the form (-COOH) in their protonated form and (-COO-) in their unprotonated form. It is this trio of carboxyl groups that lends the name "tricarboxylic acid" to this cycle. The synthesis is driven by the addition of a water molecule, making this a condensation reaction, and the loss of the coenzyme A portion of acetyl CoA.

Citrate is then rearranged into a molecule with the same atoms in a different arrangement, which is fittingly called isocitrate. This molecule then gives off a CO 2 to become the five-carbon compound α-ketoglutarate, and in the next step the same thing occurs, with α-ketoglutarate losing a CO 2 while regaining a coenzyme A to become succinyl CoA. This four-carbon molecule becomes succinate with the loss of CoA, and is subsequently rearranged into a procession of four-carbon deprotonated acids: fumarate, malate and finally oxaloacetate.

The central molecules of the Krebs cycle, then, in order, are

  • α-ketoglutarate 
  • Succinyl CoA
  • Oxaloacetate

This omits the names of the enzymes and a number of critical co-reactants, among them NAD+/NADH, the similar molecule pair FAD/FADH 2 (flavin adenine dinucleotide) and CO 2 .

Note that the amount of carbon at the same point in any cycle remains the same. Oxaloacetate picks up two carbon atoms when it combines with acetyl CoA, but these two atoms are lost in the first half of the Krebs cycle as CO 2 in successive reactions in which NAD+ is also reduced to NADH. (In chemistry, to simplify somewhat, reduction reactions add protons while oxidation reactions remove them.) Looking at the process as a whole, and examining only these two-, four-, five- and six-carbon reactants and products, it is not immediately clear why cells would engage in something like resembles a biochemical Ferris wheel, with different riders from the same population being loaded on and off the wheel but nothing changing at the end of the day except for a great many turns of the wheel.

The purpose of the Krebs cycle is more obvious when you look at what happens to hydrogen ions in these reactions. At three different points, a NAD+ collects a proton, and at a different point, FAD collects two protons. Think of protons – because of their effect on positive and negative charges – as pairs of electrons. On this view, the point of the cycle is the accumulation of high-energy electron pairs from small carbon molecules.

Diving Deeper Into the Krebs Cycle Reactions

You may notice that two critical molecules expected to be present in aerobic respiration are missing from the Krebs cycle: Oxygen (O 2 ) and ATP, the form of energy directly employed by cells and tissues to carry out work such as growth, repair and so on. Again, this is because the Krebs cycle is a table-setter for the electron transport chain reactions that occur nearby, in the mitochondrial membrane rather than in the mitochondrial matrix. The electrons harvested by nucleotides (NAD+ and FAD) in the cycle are used "downstream" when they are accepted by oxygen atoms in the transport chain. The Krebs cycle in effect strips away valuable material in a seemingly unremarkable circular conveyor belt and exports them to a nearby processing center where the real production team is at work.

Also note that the seemingly unnecessary reactions in the Krebs cycle (after all, why take eight steps to accomplish what might be done in perhaps three or four?) generate molecules that, though intermediates in the Krebs cycle, can serve as reactants in unrelated reactions.

For reference, NAD accepts a proton at Steps 3, 4 and 8, and in the first two of these CO 2 is shed; a molecule of guanosine triphosphate (GTP) is produced from GDP at Step 5; and FAD accepts two protons at Step 6. In step 1, CoA "leaves," but "returns" in Step 4. In fact, only Step 2, the rearrangement of citrate into isocitrate, is "silent" outside of the carbon molecules in the reaction.

A Mnemonic for Students

Because of the importance of the Krebs cycle in biochemistry and human physiology, students, professors and others have come up with a number of mnemonics, or ways to remember names, to help with remembering the steps and reactants in the Krebs cycle. If one only wishes to remember the carbon reactants, intermediates and products, it is possible to work from the first letters of successive compounds as they appear (O, Ac, C, I, K, Sc, S, F, M; here, notice that "coenzyme A" is represented by a small "c"). You can create a pithy personalized phrase from these letters, with the first letters of the molecules serving as the first letters in the words of the phrase.

A more sophisticated way of going about this is to use a mnemonic that lets you keep track of the number of carbon atoms at every step, which may allow you to better internalize what is happening from a biochemical standpoint at all times. For example, if you let a six-letter word represent the six-carbon oxaloacetate, and correspondingly for smaller words and molecules, you can produce a scheme that is both useful as a memory device and information rich. One contributor to the "Journal of Chemical Education" proposed the following idea :

  • Tangle 

Here, you see a six-letter word formed by a two-letter word (or group) and a four-letter word. Each of the next three steps includes a single letter substitution with no loss of letters (or "carbon"). The next two steps each involve the loss of a letter (or, again, "carbon"). The rest of the scheme preserves the four-letter word requirement in the same way the last steps of the Krebs cycle include different, closely related four-carbon molecules.

Apart from these specific devices, you may find it beneficial to draw yourself a complete cell or portion of a cell surrounding a mitochondrion, and sketch the reactions of glycolysis in as much detail as you like in the cytoplasm part and the Krebs cycle in the mitochondrial matrix part. You would, in this sketch, show pyruvate being shuttled into the interior of the mitochondria, but you could also draw an arrow leading to fermentation, which also occurs in the cytoplasm.

Related Articles

What does glycolysis yield, glycolysis: definition, steps, products & reactants, what happens when glucose enters a cell, how to metabolize glucose to make atp, what are the four phases of complete glucose breakdown, how does glycolysis occur, cellular respiration: definition, equation & steps, what is the function of aerobic respiration, what is lactic acid fermentation, what is the difference between nadh and nadph, what performs glycolysis, the difference between glycolysis and gluconeogenesis, easy ways to memorize homonuclear diatomic molecules, what is the bridge stage of glycolysis.

  • Journal of Chemical Education: A Mnemonic for the Krebs Cycle
  • Scitable by Nature Education: Nutrient Utilization in Humans: Metabolism Pathways

About the Author

Kevin Beck holds a bachelor's degree in physics with minors in math and chemistry from the University of Vermont. Formerly with ScienceBlogs.com and the editor of "Run Strong," he has written for Runner's World, Men's Fitness, Competitor, and a variety of other publications. More about Kevin and links to his professional work can be found at www.kemibe.com.

Find Your Next Great Science Fair Project! GO

We Have More Great Sciencing Articles!

How to Learn Glycolysis

MedStudy Blog

  • Internal Medicine
  • Med Student

assignment on krebs cycle

5 Reasons to Brush Up on Heart Sounds During American Heart Month

  • Behavior science
  • CME & MOC
  • Guideline updates
  • Improving patient care & outcomes
  • In-training (ITE) exams
  • Learning science
  • MedStudy products
  • Preparing for residency
  • Residency life

Subscribe Here!

Subscribe to get more marketing articles from sparkreaction:, krebs cycle study guide (that will help you actually remember it).

assignment on krebs cycle

The citric acid cycle (a.k.a. tricarboxylic acid [TCA] cycle or Krebs cycle) is arguably one of the most difficult topics to try and master in medical school or any medical profession. It's about time for a better way to study it! Follow our Krebs cycle study guide below using the MedStudy Method to remember it for the long term. 

CITRIC ACID CYCLE — OVERVIEW      |      SUBSTRATE FOR THE CITRIC ACID CYCLE      |      STEPS OF THE CITRIC ACID CYCLE       

  CITRIC ACID CYCLE INTERMEDIATES    |      SUMMARY OF ENERGY GENERATION      |      LEARN MORE 

As per the MedStudy Method , the first thing you need to do when studying a new topic is review the material. Try to dredge up everything you can about each of these Preview | Review questions before going to the reading. Then, a s you read the Krebs cycle Study Guide, the answers to these questions will be highlighted, just like in the Medical Student Core . 

Krebs Cycle Preview | Review questions from the Medical Student Digital Core

Krebs cycle Preview | Review questions from the Medical Student Digital Core

Review the Krebs cycle study guide 

After you've reviewed the Preview | Review questions, it's time to dive into the material. 

CITRIC ACID CYCLE — OVERVIEW

The citric acid cycle (a.k.a. tricarboxylic acid [TCA] cycle or Krebs cycle, for Hans Adolph Krebs who identified it in 1937) is a series of biochemical reactions used by all aerobic organisms to produce energy from carbohydrates, protein, and fat. This occurs through the oxidation of acetyl-CoA, leading to ATP production. In contrast to glycolysis, the citric acid cycle occurs in mitochondria.

This process was named the citric acid cycle because it begins with conversion of acetyl-CoA to citric acid (a.k.a. citrate). The citrate is consumed and eventually regenerated to continue the cycle. Citrate is a type of TCA.

Think of the citric acid cycle as the biochemical crossroads of the cell. First, it is the final common pathway for the oxidation of fuel, meaning carbohydrates, amino acids, and fatty acids. Any molecule that can be broken down into an acetyl group or dicarboxylic acid can enter this pathway to produce ATP. Recall that glycolysis produces only a small amount of ATP from glucose. Further processing in the citric acid cycle (in conjunction with oxidative phosphorylation) is the main source of ATP generated in metabolism, accounting for about 95% of energy in aerobic cells. Second, there are many important byproducts of the reactions in the citric acid cycle. These include precursors for amino acids, nucleotide bases, cholesterol, and porphyrin, as well as NADH and other forms of energy.

The cycle is a series of 8 enzymatic oxidation-reduction, or redox, reactions. Oxidation is a chemical reaction in which a molecule loses electrons, whereas reduction is a chemical reaction in which a molecule gains electrons. Redox reactions involve the transfer of electrons between molecules during the same reaction. Chemically, the citric acid cycle produces high-energy electrons from carbon fuel (see figure). It does this by removing electrons from acetyl-CoA and using them to generate NADH and the reduced form of flavin adenine dinucleotide (FADH2) (see figure). NADH and FADH2 transfer their electrons in the electron transport chain, and through oxidative phosphorylation, generate most of the ATP in aerobic cells. Oxygen is not used directly in the citric acid cycle. It is the final electron acceptor at the end of the electron transport chain, regenerating NAD+ and FAD.

NADH and FADH2 production in the citric acid cycle

NADH and FADH2 production in the citric acid cycle

Electron production in the citric acid cycle and use in oxidative phosphorylation

Electron production in the citric acid cycle and use in oxidative phosphorylation

SUBSTRATE FOR THE CITRIC ACID CYCLE

Once acetyl-CoA is in a mitochondrion, it cannot be transported out. There are 2 main sources of acetyl-CoA:

1) Glucose : At the end of glycolysis, the PDC converts pyruvate to acetyl-CoA.

2) Fatty acids : β-oxidation of fatty acids yields acetyl-CoA. Note that β-oxidation of some fatty acids produces propionyl-CoA, which is converted to succinyl- CoA. Succinyl-CoA can enter the citric acid cycle as an intermediate.

Did you notice that we did not mention proteins? So, how do proteins enter the citric acid cycle? Proteases break proteins down into their constituent amino acids. Their carbon skeletons can enter the citric acid cycle in a few different ways:

• By conversion into intermediates; for example, glutamine is processed to form α-ketoglutarate.

• By conversion into acetyl-CoA; this is possible for several amino acids, including leucine, isoleucine, lysine, phenylalanine, tryptophan, and tyrosine.

• By conversion into pyruvate; this is possible for alanine, cysteine, glycine, serine, and threonine.

STEPS OF THE CITRIC ACID CYCLE

Review the 8 reactions of the citric acid cycle:.

The citric acid cycle

The citric acid cycle

• Step 1: A 2-carbon unit of acetyl-CoA condenses with a 4-carbon unit of oxaloacetate to form a 6-carbon unit of citrate. ◦ Citrate synthase catalyzes this reaction.

• Step 2: Aconitase catalyzes the isomerization of citrate to isocitrate. ◦ Isocitrate is much more readily oxidized than citrate.

• Step 3: Isocitrate dehydrogenase catalyzes the oxidative decarboxylation of isocitrate. This removes a unit of CO2, resulting in a 5-carbon unit of α-ketoglutarate. ◦ This reaction requires the input of NAD+ and produces NADH.

• Step 4: The α-ketoglutarate dehydrogenase complex catalyzes the oxidative decarboxylation of α-ketoglutarate. This removes another unit of CO2, resulting in a 4-carbon unit of succinyl-CoA, which is an energy-rich compound. ◦ This reaction also requires the input of NAD+ and produces NADH.

• Step 5: Succinyl-CoA synthetase cleaves succinyl-CoA to produce succinate. ◦ This reaction is coupled with phosphorylation of guanosine diphosphate (GDP) to produce guanosine triphosphate (GTP). (Note that it is possible to convert GTP to ATP. The enzyme nucleoside diphosphokinase catalyzes the reaction of GTP + ADP → GDP + ATP.)

• Step 6: Succinate dehydrogenase oxidizes succinate to fumarate. ◦ This is a difficult oxidation reaction, so it utilizes FAD, which is a more powerful oxidant than NAD+. The FAD is reduced to FADH2.

• Step 7: Fumarase hydrates (adds H2O) fumarate to produce malate.

• Step 8: Malate dehydrogenase oxidizes malate to produce oxaloacetate. ◦ This reaction requires the input of NAD+ and produces NADH.

CITRIC ACID CYCLE INTERMEDIATES

Some of the intermediates formed in the citric acid cycle leave the cycle to enter other biosynthetic pathways. Although acetyl-CoA cannot leave the mitochondrion, citrate can. Once it is in the cytoplasm, the citrate can be converted back into acetyl-CoA for use in fatty acid and cholesterol synthesis. Likewise, malate can leave the mitochondrion. In the cytosol, malate is oxidized back to oxaloacetate, which enters the gluconeogenesis pathway.

Some intermediates provide the carbon skeletons for nonessential amino acids (i.e., amino acids the body can make, which means they do not have to be consumed in the diet). α-ketoglutarate is processed to form glutamine, proline, and arginine. Oxaloacetate is processed to form aspartate and asparagine.

Succinyl-CoA provides the carbon needed for synthesis of porphyrins, which are heterocyclic organic compounds. Porphyrins are important components of hemoglobin, myoglobin, and cytochromes.

Citric acid cycle intermediates are depleted in the reactions involving synthesis of fatty acids, cholesterol, glucose, nonessential amino acids, and porphyrins. Other processes that replenish the supply of intermediates of metabolic pathways are referred to as anaplerotic pathways. The flow of intermediates into and out of the citric acid cycle is balanced, so that concentrations of these molecules within the mitochondria remain constant over time.

SUMMARY OF ENERGY GENERATION

In a single turn of the citric acid cycle:

• 2 carbon atoms enter the cycle in the form of acetyl-CoA, and 2 molecules of CO2 are released.

• 3 NADH and 1 FADH2 are generated.

• 1 GTP is produced, which ultimately is converted to ATP.

The chemical equation representing the sum of the 8 reactions in a single turn of the citric acid cycle is:

Acetyl-CoA + 2 H 2 O + 3 NAD + + FAD + GDP + P i →

2 CO 2 + 3 NADH + 3H + + FADH 2 + uncombined coenzyme A (CoASH) + GTP

Note that 1 molecule of glucose yields 2 molecules of acetyl-CoA, so you will actually want to double the above numbers to show the yield for each molecule of glucose. So, for 1 glucose molecule, the energy output for the citric acid cycle is 2 ATP, 6 NADH, and 2 FADH2. You can see that at this point we have not generated that much more ATP than we did in glycolysis. But look at all the energy-rich NADH and FADH2 we generated! The big payoff arrives in the electron transport chain, which generates about 3 ATP per NADH oxidized and 2 ATP per FADH2 oxidized. In total, aerobic cellular respiration yields approximately 38 ATP from the oxidation of 1 molecule of glucose!

Love the conversational writing style of the Medical Student Core? Get your copy. 

Want to read even more of the of the Biochemistry section of the Student Core for FREE?   hbspt.forms.create({ region: "na1", portalId: "130734", formId: "09f21dee-14b1-4d91-bbb4-c634bdcf9076" });

Related Categories

19 physician-approved tips for how to study in medical school, everything you need to know about abim lka, the complete guide to the internal medicine board exam, get blogs straight to your inbox, sign up for our weekly newsletter, you may also like:, the complete guide to learning heart auscultation.

Key Takeaways:

What to know about S1, S2, S3, & S4 heart sounds

Key takeaways:

Tips & Tricks: 11 Qbank+ Features You Need to Know About

We're constantly refining our medical learning tools to offer you the best learning and review experience out there, and...

MedStudy-Logo-1

MedStudy makes learning medicine easier. From board prep to continuing ed, wherever you are in your medical journey, our study solutions can help you succeed.

Talk to our experts

1800-120-456-456

Krebs Cycle

Krebs cycle or citric acid cycle.

The Krebs cycle or Citric acid cycle is a series of enzyme-catalyzed reactions occurring in the mitochondrial matrix, where acetyl-CoA is oxidized to form carbon dioxide and coenzymes are reduced, which generate ATP in the electron transport chain.

Krebs cycle was named after Hans Krebs, who postulated the detailed cycle. He was awarded the Nobel prize in 1953 for his contribution.

It is a series of eight-step processes, where the acetyl group of acetyl-CoA is oxidized to form two molecules of \[CO_{2}\] and in the process, one ATP is produced. Reduced high-energy compounds, NADH, and \[FADH_{2}\] are also produced.

Two molecules of acetyl-CoA are produced from each glucose molecule so two turns of the Krebs cycle are required which yields four \[CO_{2}\], six NADH, two FADH₂, and two ATPs.

Krebs Cycle is a Part of Cellular Respiration

Cellular respiration is a catabolic reaction taking place in the cells. It is a biochemical process by which nutrients are broken down to release energy, which gets stored in the form of ATP, and waste products are released. In aerobic respiration, oxygen is required.

Cellular respiration is a four-stage process. In the process, glucose is oxidized to carbon dioxide and oxygen is reduced to water. The energy released in the process is stored in the form of ATPs. 36 to 38 ATPs are formed from each glucose molecule.

The Four Stages are

Glycolysis: Partial oxidation of a glucose molecule to form 2 molecules of pyruvate. This process takes place in the cytosol.

Formation of Acetyl CoA: Pyruvate formed in glycolysis enters the mitochondrial matrix. It undergoes oxidative decarboxylation to form two molecules of Acetyl CoA. The reaction is catalyzed by the pyruvate dehydrogenase enzyme.

\[2Pyruvate + 2NAO^{-} + 2CoA^{-} \overset{ Pyruvate dehydrogenase }{\rightarrow} 2 Acetyl CoA + 2NADH + C0_{2}\]

Krebs Cycle (TCA or Citric Acid Cycle): It is the common pathway for complete oxidation of carbohydrates, proteins, and lipids as they are metabolized to acetyl coenzyme A or other intermediates of the cycle. The Acetyl CoA produced enters the Tricarboxylic acid cycle or Citric acid cycle. Glucose is fully oxidized in this process. The acetyl CoA combines with oxaloacetate (4C) to form citrate (6C). In this process, 2 molecules of \[CO_{2}\] are released and oxaloacetate is recycled. Energy is stored in ATP and other high-energy compounds like NADH and \[FADH_{2}\].

Electron Transport System and Oxidative Phosphorylation: ATP is generated when electrons are transferred from the energy-rich molecules like NADH and \[FADH_{2}\] produced in glycolysis, citric acid cycle, and fatty acid oxidation to molecular \[O_{2}\] by a series of electron carriers. \[O_{2}\] is reduced to \[H_{2}O\]. It takes place in the inner membrane of mitochondria.

Krebs Cycle Steps

It is an eight-step process. The Krebs cycle takes place in the matrix of mitochondria under aerobic conditions.

Step 1: The first step is the condensation of acetyl CoA with oxaloacetate (4C) to form citrate (6C), coenzyme A is released. The reaction is catalyzed by citrate synthase.

Step 2: Citrate is turned to its isomer, isocitrate. The enzyme aconitase catalyzes this reaction. 

Step 3: Isocitrate undergoes dehydrogenation and decarboxylation to form 𝝰-ketoglutarate (5C). A molecular of \[CO_{2}\] is released. Isocitrate dehydrogenase catalyzes the reaction. It is an NAD+-dependent enzyme. NAD+ is converted to NADH.

Step 4: α-ketoglutarate (5C) undergoes oxidative decarboxylation to form succinyl CoA (4C). The reaction is catalyzed by the α-ketoglutarate dehydrogenase enzyme complex. One molecule of \[CO_{2}\] is released and NAD+ is converted to NADH.

Step 5: Succinyl CoA is converted to succinate by the enzyme succinyl CoA synthetase. This is coupled with substrate-level phosphorylation of GDP to form GTP. GTP transfers its phosphate to ADP forming ATP.

Step 6: Succinate is oxidized to fumarate by the enzyme succinate dehydrogenase. In the process, FAD is converted to \[FADH_{2}\].

Step 7: Fumarate gets converted to malate by the addition of one \[H_{2}O\]. The enzyme catalyzing this reaction is fumarase.

Step 8: Malate is dehydrogenated to form oxaloacetate, which combines with another molecule of acetyl CoA and starts the new cycle. Hydrogens removed get transferred to NAD+ forming NADH. Malate dehydrogenase catalyzes the reaction.

Krebs Cycle Summary

Location: Krebs cycle occurs in the mitochondrial matrix

Krebs Cycle Reactants: Acetyl CoA, which is produced from the end product of glycolysis, i.e. pyruvate and it condenses with 4 carbon oxaloacetate, which is generated back in the Krebs cycle.

Krebs Cycle Products

Each citric acid cycle forms the following products:

2 molecules of \[CO_{2}\] are released. Removal of \[CO_{2}\] or decarboxylation of citric acid takes place at two places:

In the conversion of isocitrate (6C) to α-ketoglutarate (5C)

In the conversion of α-ketoglutarate (5C) to succinyl CoA (4C)

1 ATP is produced in the conversion of succinyl CoA to succinate

3 NAD+ are reduced to NADH and 1 FAD+ is converted to \[FADH_{2}\] in the following reactions:

Isocitrate to α-ketoglutarate → NADH

α-ketoglutarate to succinyl CoA → NADH

Succinate to fumarate → \[FADH_{2}\]

Malate to Oxaloacetate → NADH

Notes that 2 molecules of Acetyl CoA are produced from oxidative decarboxylation of 2 pyruvates so two cycles are required per glucose molecule.

To summarize, for complete oxidation of a glucose molecule, the Krebs cycle yields \[ 4 CO_{2}, 6NADH, 2 FADH_{2} \], and 2 ATPs.

Each molecule of NADH can form 2-3 ATPs and each FADH₂ gives 2 ATPs on oxidation in the electron transport chain.

Krebs Cycle Equation

\[ 2  Acytyl  CoA + 6 NAO^{-} + 2 FAD + 2ADP + 2P_{i} + 2H_{2}0  \rightarrow  4CO_{2} + 6 NADH + 2FADH_{2} + 2ATP + CoA \]

Significance of Krebs Cycle

The Krebs cycle or Citric acid cycle is the final pathway of oxidation of glucose, fats, and amino acids.

Many animals are dependent on nutrients other than glucose as an energy source.

Amino acids (metabolic product of proteins) are deaminated and get converted to pyruvate and other intermediates of the Krebs cycle. They enter the cycle and get metabolized e.g. alanine is converted to pyruvate, glutamate to α-ketoglutarate, aspartate to oxaloacetate on deamination.

Fatty acids undergo β-oxidation to form acetyl CoA, which enters the Krebs cycle.

It is the major source of ATP production in the cells. A large amount of energy is produced after the complete oxidation of nutrients.

It plays an important role in gluconeogenesis lipogenesis and interconversion of amino acids.

Many intermediate compounds are used in the synthesis of amino acids, nucleotides, cytochromes, chlorophylls, etc.

Vitamins play an important role in the citric acid cycle. Riboflavin, niacin, thiamin, and pantothenic acid a part of various enzymes cofactors (FAD, NAD) and coenzyme A.

Regulation of the Krebs cycle depends on the supply of NAD+ and the utilization of ATP in physical and chemical work.

The genetic defects of the Krebs cycle enzymes are associated with neural damage.

As most of the processes occur in the liver to a significant extent, damage to liver cells has a lot of repercussions. Hyperammonemia occurs in liver diseases and leads to convulsions and coma. This is due to reduced ATP generation as a result of the withdrawal of α-ketoglutarate and the formation of glutamate, which forms glutamine.

FAQs on Krebs Cycle

1. What is the Krebs Cycle?

Also known as the citric acidity cycle, Kreb’s cycle is a chain of reactions occurring in the mitochondria, through which almost all living cells produce energy in aerobic respiration. It consumes oxygen to give out water and carbon dioxide is the product. Here, ADP is converted into ATP. This cycle renders electrons and hydrogen required for electron chain transport.

2. How Many ATP are Produced in Krebs Cycle?

2 ATPs are produced in one Krebs Cycle. For complete oxidation of a glucose molecule, the Krebs cycle yields \[4 CO_{2}\], 6NADH, \[2 FADH_{2}\], and 2 ATPs.

3. Where Does Krebs Cycle Occur?

Mitochondrial matrix. In all eukaryotes, mitochondria are the site where the Krebs cycle takes place. The cycle takes place in a mitochondrial matrix producing chemical energy in the form of NADH, ATP, \[FADH_{2}\]. These are produced as a result of oxidation of the end product of glycolysis – pyruvate.

4. How does the Krebs Cycle Works?

It is an Eight-Step Process

Condensation of acetyl CoA with oxaloacetate (4C) forming citrate (6C), coenzyme A is released.

Conversion of Citrate to its isomer, isocitrate.

Isocitrate is subjected to dehydrogenation and decarboxylation forming α-ketoglutarate (5C). 

α-ketoglutarate (5C) experiences oxidative decarboxylation forming succinyl CoA (4C). 

Conversion of Succinyl CoA to succinate by succinyl CoA synthetase enzyme along with substrate-level phosphorylation of GDP forming GTP.

Fumarate gets converted to malate by the addition of one \[H_{2}O\]. 

Malate is dehydrogenated to form oxaloacetate, which combines with another molecule of acetyl CoA and starts the new cycle.

5. Why is Krebs Cycle Called an Amphibolic Pathway?

It is called amphibolic as in the Krebs cycle both catabolism and anabolism take place. The amphibolic pathway indicates the one involving both catabolic and anabolic procedures.

6. What is the Krebs cycle?

The Krebs cycle is a process that occurs in one of the most significant reaction sequences in biochemistry is the Krebs cycle, commonly known as the citric acid cycle or the tricarboxylic acid cycle. Not only are the molecules produced in these reactions responsible for the majority of the energy needs in complex organisms, but they can also be used as building blocks for a lot of crucial processes. Synthesis of fatty acids, steroids, cholesterol, amino acids for protein building, and the purines and pyrimidines are used in DNA synthesis. Lipids (fats) and carbohydrates, which both create the chemical acetyl coenzyme-A, provide energy for the Krebs cycle (acetyl-CoA).

This acetyl-CoA reacts in the first of the eight steps that make up the Krebs cycle, which all take place inside the mitochondria of eukaryotic cells. As the Krebs cycle produces carbon dioxide, it does not directly generate significant chemical energy in the form of adenosine triphosphate (ATP), nor does it make the use of oxygen necessary. This cycle produces NADH and \[FADH_{2}\] , which are fed into the respiratory cycle, which is likewise confined inside the mitochondria. 

The process of the citric acid cycle takes place in the matrix of the mitochondria in eukaryotic cells. The citric acid cycle reaction sequence takes place in the cytosol in prokaryotic cells without mitochondria, like bacteria, with the proton gradient for ATP synthesis being across the cell rather than the inner membrane of the mitochondrion. The TCA cycle produces three NADH, one \[FADH_{2}\] , and one GTP as a total yield of energy-containing molecules.

7. What is the biochemistry of muscle mitochondria?

The hydrogen atoms (or the electrons derived from them) do not react directly with oxygen in the Krebs cycle oxidation processes; instead, they transit via a succession of hydrogen or electron carriers, known as the respiratory chain.

The lipoic acid covalently linked to one of the proteins of the corresponding keto–acid dehydrogenase complex is the major hydrogen acceptor for the oxidation of pyruvate and -ketoglutarate. In a process catalyzed by lipoamide dehydrogenase, hydrogens from reduced lipoic acid are transported to NAD+. NAD+ also functions as a hydrogen acceptor for the oxidation of a lot of substrates. Malate, isocitrate, and l-3-hydroxy acyl-CoA, with each oxidoreduction, get mediated by a different dehydrogenase.

8. What is the biochemistry of muscle mitochondria?

The steps in the Krebs cycle are:

The TCA cycle starts with an enzymatic aldol addition reaction of acetyl CoA to oxaloacetate, which results in the formation of citrate.

A dehydration-hydration sequence is used to isomerize citrate, yielding (2R,3S)-isocitrate.

2-ketoglutarate is formed after more enzymatic oxidation and decarboxylation.

2-ketoglutarate is converted to succinyl-CoA after more enzymatic decarboxylation and oxidation.

The phosphorylation of guanosine diphosphate (GDP) to guanosine triphosphate is connected to the hydrolysis of this metabolite to succinate (GTP).

Fumarate is generated by the enzyme flavin adenine dinucleotide (FAD)-dependent succinate dehydrogenase.

Fumarate catalyzed by fumarase is changed to L-malate after going through stereospecific hydration.

Malate dehydrogenase catalyzes the final step of NAD-coupled oxidation of L-malate to oxaloacetate, which completes the cycle.

9. What is the efficiency of the Krebs cycle?

The theoretical maximal yield of ATP from glycolysis, the citric acid cycle, and oxidative phosphorylation is 38. Glycolysis, which occurs in the cytoplasm of eukaryotes, produces two equivalents of NADH and four equivalents of ATP. The transport of two equivalents of NADH into the mitochondria uses two equivalents of ATP, lowering the net ATP production to 36. Furthermore, oxidative phosphorylation inefficiencies caused by proton leakage across the mitochondrial membrane and ATP synthase/proton pump slippage typically lower ATP yield from NADH and   \[FADH_{2}\] , to less than the theoretical maximum output. As a result, the observed yields are closer to 2.5 ATP per NADH and 1.5 ATP per \[FADH_{2}\] ,  lowering the total net ATP generation to around 30.

Based on freshly revised proton-to-ATP ratios, the total ATP yield is estimated to be 29.85 ATP per glucose molecule.

10. What is the role of the Krebs cycle in the metabolism of carbohydrates?

The role of mitochondria in oxidative phosphorylation has already been discussed, as has their role in carbohydrate metabolism due to the presence of enzymes involved in the Krebs cycle and cytochrome system in their substance. Then, we should brood regarding glucose metabolism and the role that mitochondria and other cytoplasm components have in it.

Carbohydrate metabolism is critical for cell synthesis and serves as the primary source of energy for cell functions. Before we try to pinpoint where the various functions of glucose metabolism occur in the cell, let's have a look at what carbohydrate metabolism entails. Anaerobic and aerobic metabolism are the two forms of metabolism. Head to the Vedantu app and website for free study materials.

Biology • Class 11

  • NEET Study Material
  • NEET Biology

Krebs Cycle

Cellular Respiration Steps Products Significance Frequently Asked Questions

Introduction

The Krebs cycle or TCA cycle (tricarboxylic acid cycle) or Citric acid cycle is a series of enzyme catalysed reactions occurring in the mitochondrial matrix, where acetyl-CoA is oxidised to form carbon dioxide and coenzymes are reduced, which generate ATP in the electron transport chain.

Download Complete Chapter Notes of Respiration in Plants Download Now

Also see: NEET Key Answer 2022

Krebs cycle was named after Hans Krebs, who postulated the detailed cycle. He was awarded the Nobel prize in 1953 for his contribution.

It is a series of eight-step processes, where the acetyl group of acetyl-CoA is oxidised to form two molecules of CO 2 and in the process, one ATP is produced. Reduced high energy compounds, NADH and FADH 2 are also produced.

Two molecules of acetyl-CoA are produced from each glucose molecule so two turns of the Krebs cycle are required which yields four CO 2 , six NADH, two FADH 2 and two ATPs.

Krebs Cycle is a part of Cellular Respiration

Cellular respiration is a catabolic reaction taking place in the cells. It is a biochemical process by which nutrients are broken down to release energy, which gets stored in the form of ATP and waste products are released. In aerobic respiration, oxygen is required.

Also see: Biochemical Pathways

Cellular respiration is a four-stage process. In the process, glucose is oxidised to carbon dioxide and oxygen is reduced to water. The energy released in the process is stored in the form of ATPs. 36 to 38 ATPs are formed from each glucose molecule.

The four stages are:

1. Glycolysis: Partial oxidation of a glucose molecule to form 2 molecules of pyruvate. This process takes place in the cytosol.

Further reading:  Significance of Glycolysis

2. Formation of Acetyl CoA: Pyruvate formed in glycolysis enters the mitochondrial matrix. It undergoes oxidative decarboxylation to form two molecules of Acetyl CoA. The reaction is catalysed by the pyruvate dehydrogenase enzyme.

3. Krebs cycle (TCA cycle or Citric Acid Cycle): It is the common pathway for complete oxidation of carbohydrates, proteins and lipids as they are metabolised to acetyl coenzyme A or other intermediates of the cycle. The Acetyl CoA produced enters the Tricarboxylic acid cycle or Citric acid cycle. Glucose is fully oxidized in this process. The acetyl CoA combines with 4-carbon compound oxaloacetate to form 6C citrate. In this process, 2 molecules of CO 2 are released and oxaloacetate is recycled. Energy is stored in ATP and other high energy compounds like NADH and FADH 2 .

4. Electron Transport System and Oxidative Phosphorylation: ATP is generated when electrons are transferred from the energy-rich molecules like NADH and FADH 2 , produced in glycolysis, citric acid cycle and fatty acid oxidation to molecular O 2 by a series of electron carriers. O 2 is reduced to H 2 O. It takes place in the inner membrane of mitochondria.

Also Check: MCQs on Krebs Cycle

Krebs Cycle Steps

It is an eight-step process. Krebs cycle or TCA cycle takes place in the matrix of mitochondria under aerobic condition.

Step 1:  The first step is the condensation of acetyl CoA with 4-carbon compound oxaloacetate to form 6C citrate, coenzyme A is released. The reaction is catalysed by citrate synthase .

Step 2: Citrate is converted to its isomer, isocitrate. The enzyme aconitase catalyses this reaction.

Step 3: Isocitrate undergoes dehydrogenation and decarboxylation to form 5C 𝝰-ketoglutarate. A molecular form of CO 2 is released. Isocitrate dehydrogenase catalyses the reaction. It is an NAD + dependent enzyme. NAD + is converted to NADH.

Step 4: 𝝰-ketoglutarate undergoes oxidative decarboxylation to form succinyl CoA, a 4C compound. The reaction is catalyzed by the  𝝰-ketoglutarate dehydrogenase enzyme complex. One molecule of CO 2 is released and NAD + is converted to NADH.

Step 5: Succinyl CoA forms succinate. The enzyme succinyl CoA synthetase catalyses the reaction. This is coupled with substrate-level phosphorylation of GDP to get GTP. GTP transfers its phosphate to ADP forming ATP.

Step 6: Succinate is oxidised by the enzyme succinate dehydrogenase  to fumarate. In the process, FAD is converted to FADH 2 .

Step 7: Fumarate gets converted to malate by the addition of one H 2 O. The enzyme catalysing this reaction is fumarase .

Step 8: Malate is dehydrogenated to form oxaloacetate, which combines with another molecule of acetyl CoA and starts the new cycle. Hydrogens removed, get transferred to NAD + forming NADH. Malate dehydrogenase catalyses the reaction.

Krebs Cycle

Krebs Cycle Summary

Location: Krebs cycle occurs in the mitochondrial matrix

Krebs cycle reactants: Acetyl CoA, which is produced from the end product of glycolysis, i.e. pyruvate and it condenses with 4 carbon oxaloacetate, which is generated back in the Krebs cycle

Krebs cycle products

Each citric acid cycle forms the following products:

  • In the conversion of isocitrate (6C) to 𝝰-ketoglutarate (5C)
  • In the conversion of 𝝰-ketoglutarate (5C) to succinyl CoA (4C)
  • 1 ATP is produced in the conversion of succinyl CoA to succinate
  • Isocitrate to 𝝰-ketoglutarate → NADH
  • 𝝰-ketoglutarate to succinyl CoA → NADH
  • Succinate to fumarate → FADH 2
  • Malate to Oxaloacetate → NADH

Note that 2 molecules of Acetyl CoA are produced from oxidative decarboxylation of 2 pyruvates so two cycles are required per glucose molecule.

To summarize, for complete oxidation of a glucose molecule, Krebs cycle yields 4 CO 2 , 6NADH, 2 FADH 2 and 2 ATPs.

Each molecule of NADH can form 2-3 ATPs and each FADH 2 gives 2 ATPs on oxidation in the electron transport chain.

Krebs cycle equation

Significance of Krebs Cycle

  • Krebs cycle or Citric acid cycle is the final pathway of oxidation of glucose, fats and amino acids
  • Many animals are dependent on nutrients other than glucose as an energy source
  • Amino acids (metabolic product of proteins) are deaminated and get converted to pyruvate and other intermediates of the Krebs cycle. They enter the cycle and get metabolised e.g. alanine is converted to pyruvate, glutamate to 𝝰-ketoglutarate, aspartate to oxaloacetate on deamination
  • Fatty acids undergo 𝞫-oxidation to form acetyl CoA, which enters the Krebs cycle
  • It is the major source of ATP production in the cells. A large amount of energy is produced after complete oxidation of nutrients
  • It plays an important role in gluconeogenesis and lipogenesis and interconversion of amino acids
  • Many intermediate compounds are used in the synthesis of amino acids, nucleotides, cytochromes and chlorophylls, etc.
  • Vitamins play an important role in the citric acid cycle. Riboflavin, niacin, thiamin and pantothenic acid as a part of various enzymes cofactors (FAD, NAD) and coenzyme A
  • Regulation of Krebs cycle depends on the supply of NAD + and utilization of ATP in physical and chemical work
  • The genetic defects of the Krebs cycle enzymes are associated with neural damage
  • As most of the biological processes occur in the liver to a significant extent, damage to liver cells has a lot of repercussions. Hyperammonemia occurs in liver diseases and leads to convulsions and coma. This is due to reduced ATP generation as a result of the withdrawal of 𝝰-ketoglutarate and formation of glutamate, which forms glutamine

Frequently Asked Questions on Krebs Cycle

What is the krebs cycle.

Also known as the citric acid cycle, the Krebs cycle or TCA cycle is a chain of reactions occurring in the mitochondria, through which almost all living cells produce energy in aerobic respiration. It uses oxygen and gives out water and carbon dioxide as products. Here, ADP is converted into ATP. This cycle renders electrons and hydrogen required for electron chain transport.

How Many ATPs are Produced In the Krebs Cycle?

2 ATPs are produced in one Krebs Cycle. For complete oxidation of a glucose molecule, the Krebs cycle yields 4 CO2, 6NADH, 2 FADH2 and 2 ATPs.

Where Does Krebs Cycle or TCA cycle Occur?

Mitochondrial matrix. In all eukaryotes, mitochondria are the site where the Krebs cycle takes place. The cycle takes place in a mitochondrial matrix producing chemical energy in the form of NADH, ATP, FADH2. These are produced as a result of oxidation of the end product of glycolysis – pyruvate.

How The Krebs Cycle Works?

It is an eight-step process 1) Condensation of acetyl CoA with oxaloacetate (4C) forming citrate (6C), coenzyme A is released. 2) Conversion of Citrate to its isomer, isocitrate. 3) Isocitrate is subjected to dehydrogenation and decarboxylation forming 𝝰-ketoglutarate (5C). 4) 𝝰-ketoglutarate (5C) experiences oxidative decarboxylation forming succinyl CoA (4C). 5) Conversion of Succinyl CoA to succinate by succinyl CoA synthetase enzyme along with substrate-level phosphorylation of GDP forming GTP. 6) Oxidation of Succinate to fumarate by the enzyme succinate dehydrogenase. 7) Fumarate gets converted to malate by the addition of one H2O. 8) Malate is dehydrogenated to form oxaloacetate, which combines with another molecule of acetyl CoA and starts the new cycle.

Why Is Krebs Cycle Called As Amphibolic Pathway?

It is called amphibolic as in the Krebs cycle both catabolism and anabolism take place. The amphibolic pathway indicates the one involving both catabolic and anabolic procedures.

How Many NADH are Produced In The Krebs Cycle?

3 NADH molecules

In one turn of the Krebs cycle, 3 molecules of NADH are produced. For complete oxidation of a glucose molecule, Krebs cycle yields 4 CO2, 6NADH, 2 FADH2 and 2 ATPs.

What Is The Krebs Cycle Also Known As?

Krebs cycle is also known as Citric acid cycle (CAC) or TCA cycle (tricarboxylic acid cycle)

Why Krebs Cycle Is Called the Citric Acid Cycle?

Krebs cycle is also referred to as the Citric Acid Cycle. Citric acid is the first product formed in the cycle.

Also Check:

NEET Flashcards: Respiration In Plants

NEET Flashcards: Breathing And Exchange Of Gases

NEET Flashcards: Body Fluids And Circulation

NEET Flashcards: Neural Control And Coordination

NEET Flashcards: Chemical Coordination And Integration

Recommended Video:

assignment on krebs cycle

Put your understanding of this concept to test by answering a few MCQs. Click ‘Start Quiz’ to begin!

Select the correct answer and click on the “Finish” button Check your score and answers at the end of the quiz

Visit BYJU’S for all Biology related queries and study materials

Your result is as below

Request OTP on Voice Call

Leave a Comment Cancel reply

Your Mobile number and Email id will not be published. Required fields are marked *

Post My Comment

assignment on krebs cycle

This is awesome ! It’s easy to understand things .

Super, thank you mam, sir 🙏🙏❤👉🍯😘

assignment on krebs cycle

  • Share Share

Register with Aakash BYJU'S & Download Free PDFs

Register with byju's & watch live videos.

Live Support

PraxiLabs A virtual world of science

assignment on krebs cycle

The Krebs Cycle | A Step by Step Explanations

Last Updated on May 25, 2023 by Sara Assem

You’ve probably heard the phrase Krebs cycle thrown around before. If you’re at all interested in biology, general science, etc. Then you know that the Krebs cycle has a vital role inside our bodies. But what exactly is it? Why does it deserve such an important name? You know what I’m talking about — The Krebs Cycle.

The Krebs cycle is a series of chemical reactions that help break down and release energy stored in food. The Krebs cycle is also known as the tricarboxylic acid (TCA) cycle or the citric acid cycle. The Krebs cycle is often considered to be the central hub of cellular metabolism, performing many important biochemical reactions that ultimately produce ATP.

This article takes a closer look at the Krebs cycle steps, how it works, what is the purpose of it, its diagram, also where does Krebs cycle occur, its products and more. Read our article and get all your questions answered with step by step explanations.

Table of Contents

What Is the Krebs Cycle?

Krebs Cycle

The Krebs cycle definition is a sequence of chemical reactions that occur in the body. The cycle starts with the intake of food, which is broken down into small molecules by the stomach and intestines. These molecules are then absorbed by the body through the small intestines and transported to the liver via the bloodstream. In the liver, the molecules are broken down further into smaller pieces called amino acids .

In the next step of the cycle, these amino acids are converted into glucose through a series of chemical reactions called phosphorylation. Then, the glucose enters the main cells of the body and can be used for energy or can be stored as glycogen for later use. When the body needs more energy, it stores the excess glucose as glycogen.

Glycogen is a form of starch stored in the liver and muscles that is used by the body for energy during periods of fasting or when no food is eaten for an extended period of time. If the body has excess energy after using up its supply of glycogen, it can then break down the remaining stored fat into fatty acids.

Where Does the Krebs Cycle Take Place?

the mitochondrial matrix

The Krebs cycle takes place exactly in (the mitochondrial matrix) and converts mitochondrial pyruvate into carbon dioxide and water. The mitochondrial matrix is a dense solution that surrounds the crests of the mitochondria. This matrix contains water, all the needed enzymes, coenzymes , and phosphates which are necessary for the Krebs cycle reactions.

The Main Purpose of Krebs Cycle

Briefly the purpose of the Krebs cycle is to combine carbon dioxide and water using energy from the electron transport chain. The resulting molecules are then used for the purposes of generating energy and building cells.

electron transport chain

We can also say that the purpose of the Krebs cycle is to help cells convert glucose into energy and provide ATP, which is one unit of energy. The beginning of the end-products are very high energy and end up being used as ATP in your cells.

Note: ATP or adenosine triphosphate is a substance found in all living cells that is used to provide energy for many metabolic processes and also used for making RNA molecules. It is considered as a coenzyme that works with many enzymes inside our bodies.

ATP or adenosine triphosphate structure

Glucose is a simple sugar that is found in most foods. Cells use glucose to make energy, which they need to do everything from stay alive to carrying out important chemical reactions.

Krebs Cycle Diagram

The following diagram is Krebs cycle diagram in detail, showing the different steps, structures of the intermediates through the cycle, the enzymes and coenzymes which catalyze each step in the TCA cycle.

Krebs Cycle Diagram

Krebs Cycle Steps

Now we will get all your questions answered with step by step explanations of Krebs cycle.

TCA cycle begins by breaking down pyruvate and releasing CO2 as a byproduct. This carbon can then enter different pathways depending on what type of molecule it bonds with, either O2 or NAD+ . The results of this reaction are used for ATP formation as well as for acetyl CoA formation.

Look at the previous diagram and check the following steps!

Kreps cycle occurs over eight steps:

Step 1 ( Citrate Formation)

  Acetyl CoA reacts with oxaloacetate in the presence of citrate synthase enzyme to form citrate or citric acid.

Step 2 ( Citrate Isomers Formation)

In the second step, citric acid is first converted to an intermediate compound called cis-aconitate, then converted to isocitrate which is an isomer of citrate in the presence of aconitase enzyme.

·   Step 3 ( Isocitrate decarboxylation and oxidation)

In the third step, Isocitrate compound is oxidized to form alpha-ketoglutarate in the presence of isocitrate dehydrogenase enzyme. As a result of this step, carbon dioxide is released and a NADH molecule is formed.

Step 4 ( Succinyl-CoA Formation)

In the fourth step, the Alpha-ketoglutarate compound is oxidized and binds to coenzyme A, to form succinyl CoA in the presence of a-Ketoglutarate Dehydrogenase enzyme which liberates:

  •   Second molecule of NADH
  •   Carbon dioxide

Step 5 ( GTP Production)

In the fifth step, Succinyl CoA is converted to succinate compound in the presence of Succinyl-CoA synthetase enzyme which forms a molecule of GTP through the process of GDP phosphorylation. So we can consider that the result of this step is releasing GTP molecules, the Coenzyme A and also the formation of succinate.

GTP structure

    Step 6 (Fumarate Formation)

In the sixth step, succinate compound is oxidized and converted to fumarate in the presence of Succinate Dehydrogenase enzyme. In this step, FADH₂ molecule is produced

Step 7 ( Malate Formation)

In the seventh step, Fumarate compound is converted to malate in the presence of fumarase enzyme. In this step, H2O is incorporated to form the structure of the final product (malate) so we can consider fumarase enzyme as hydrolase enzyme.

Step 8 (Oxaloacetate Formation)

In the eighth and final step, Malate compound is converted to oxaloacetate in the presence of malate Dehydrogenase enzyme. Here the NADH molecule no.3 in the cycle is produced.

We will explain the role of each enzyme in the following paragraphs.

Krebs Cycle Products

The Krebs cycle is a series of chemical reactions that allow cells to use energy from carbohydrates. The cycle starts with the entry of glucose into the cell. This energy is used for different cellular processes such as synthesizing proteins and membranes and sustaining cellular functions.

It  produces carbon dioxide and water as waste products. In order to use the energy from glucose for these processes, it has to be converted into another type of energy—in the form of adenosine triphosphate (ATP). This is the main form of energy storage in the cell and provides the cells with the energy they need to carry out various processes. The energy produced by the conversion of glucose into ATP is called cellular respiration. The Krebs cycle is an essential part of the process of cellular respiration.

The Krebs cycle also produces NADH and FADH₂ molecules, which are used in oxidative phosphorylation to produce ATP. It also produces two carbon dioxide molecules per turn (one CO2 is produced when 1 of the 4 carbons in the citric acid molecule is oxidized). The cycle produces 3 hydrogen ions (H+) during each turn.

So we can say that the net of each Krebs cycle products are:

  •   3 NADH molecules.
  • 1 FADH₂ molecule.
  • 1 GTP molecule.
  • 2 CO2 or carbon dioxide molecules.
  • 3 (H+) hydrogen ions.

Krebs Cycle Products

Note: In the case of 1 molecule of glucose, there are 2 acetyl-CoA molecules entering the Krebs cycle, so the total energy (products of the Krebs cycle) are duplicated into 6 NADH molecules /2 FADH₂ molecules / 2GTP molecules.

In the electron transport chain, each NADH molecule gives 2-3 ATPs and each FADH 2 molecule forms 2 ATPs on oxidation

  Krebs Cycle Equation (Krebs cycle formula)

The following equation is the total Krebs cycle equation or the Krebs cycle formula which describes all the results compound:

2 acetyl groups + 6 NAD + + 2 FAD + 2 ADP + 2 Pi + 2 H20————– 4CO2 + 6 NADH + 2 FADH2 + 2ATP + 2 CoA

Get a guided science lab simulation practice and go beyond the learning outcomes you’re looking for by using our PraxiLabs virtual labs for free now !

How Much ATP does the Krebs Cycle Produce?

The short answer is one molecule of ATP \ pyruvate molecule

Each molecule of pyruvate  enters citric acid cycle, forms one ATP molecule when succinyl-CoA converts to succinate in the presence of  Succinyl CoA synthetase enzyme. and there are 2 molecules of pyruvate results from the process of (one glucose) glycolysis.

So, we will have 2 molecules of ATP by the end of Krebs cycle.

 The Role of Enzymes in Krebs Cycle

Enzymes, which are proteins that catalyze chemical reactions in the body, are key players in the Krebs cycle and their role is essential for oxidative phosphorylation to occur. They regulate all the steps of the cycle.

The most well-known enzymes that are involved in the Krebs cycle:

  • Citrate synthase enzyme

Citrate synthase removes the acetyl group and then adds it to oxaloacetate compound to form citric acid.

  • Aconitase enzyme

Aconitase transfers an oxygen atom to make a more reactive molecule of isocitrate.

  •  Isocitrate dehydrogenase enzyme

Isocitrate dehydrogenase removes only one carbon atom to form carbon dioxide CO2 and also transfers the electrons to the NADH molecule.

  •   Alpha-Ketoglutarate Dehydrogenase enzyme

Alpha-Ketoglutarate Dehydrogenase removes only one carbon atom to form carbon dioxide CO2, also transfers the electrons to NADH molecule and the molecule remaining part is connected to coenzyme A.

  •   Succinyl-CoA synthetase enzyme

Because the bond between coenzyme A and succinate is unstable and needed to provide the energy for building ATP molecule, the succinyl-CoA synthetase enzyme is used to create the GTP molecule in the reaction (fifth step).

  •    Succinate Dehydrogenase enzyme

Succinate dehydrogenase plays a role in the electron transport chain by extracting the atoms of hydrogen from succinate compounds and transferring them to the FAD molecule which acts as carrier.

  •  Fumarase enzyme

Fumarase adds a molecule of water to the molecule to prepare it for the last step of citric acid cycle.

  •  Malate dehydrogenase enzyme

Malate dehydrogenase is used in the final step for oxaloacetate recreation and electrons transferring to NADH by converting malate compound to oxaloacetate compound.

Krebs Cycle Function

Krebs cycle or citric acid cycle plays a very important role in the production of energy and the molecules biosynthesis processes. The cycle ends the process of sugar-breaking which began in glycolysis and fuels the ATP production. It is also vital in the biosynthetic reactions by providing intermediates compounds that are used to synthesize important biological molecules like the amino acids. The cycle provides the electrons that fuel the oxid ative phosphorylation process which is considered as the major source of energy and ATP.

Regulation of Krebs Cycle

The TCA Cycle is regulated by many factors:

  • Enzymes, there are 3 major dehydrogenase enzymes are used for regulation in Krebs pathway:

– Pyruvate Dehydrogenase

– Isocitrate Dehydrogenase

                   – Alpha Ketoglutarate Dehydrogenase

  •  Metabolites, such as NADH which inhibits the majority of the enzymes found in the Krebs cycle and can slow and stop the process of glycolysis before the release of too much energy by the process of gluconeogenesis.
  •  Another important regulator is citrate, which inhibits phosphofructokinase and is considered as a very vital enzyme in the glycolysis process. citrate decreases the production of pyruvate and therefore acetyl-CoA (an important precursor for fat synthesis.)
  • Calcium also plays a role in the regulation of the citric acid cycle as it stimulates the link reaction and then accelerates the cycle.

Fast Facts about Krebs Cycle

Fast Facts about Krebs Cycle

  • The Krebs cycle is a cycle and a cyclic process. but it different from any other type of fuel cells as they are cyclic and rely on oxygen to synthesize energy instead of using oxygen transported by breathing.
  • The Krebs cycle gets its name because it was discovered by a scientist named Hans Adolf Krebs in 1937.
  • Krebs cycle is a metabolic pathway. It’s really a series of reactions that occur in both plant and animal cells.
  • The Krebs Cycle describes the last step of cellular respiration wherein glucose, with the help of oxygen from the lungs or bloodstream, is broken down into carbon dioxide and water.
  • In the first part of the cellular respiration, glycolysis occurs where one molecule of glucose converts into two molecules of pyruvate. These two molecules then enter the citric acid cycle which results in the formation of CO2, NADH and FADH2. They are then transported through oxidative phosphorylation to form ATP (producing 36 ATP per glucose molecule at maximum efficiency).
  • Vitamins like thiamin, riboflavin, pantothenic and niacin play a vital role in the TCA cycle, as a part of various enzyme cofactors like FAD, NAD molecules and coenzyme A.
  • Krebs cycle is known as an amphibolic (both anabolic and catabolic pathway)  process because in the cycle both anabolism and catabolism occur.
  • The Krebs Cycle is a part of cellular respiration which helps cells break down food to create energy. This process is called oxidation. The food that we eat and drink provides our bodies with energy in the form of glucose.
  • Glucose enters the cell by diffusion and this can occur at the plasma membrane or the lysosome membrane.
  • Once the sugar molecule reaches the cell membrane, the cell membrane protein pumps the sugar into the cell, across the cell wall, and into the intracellular space. Once inside the cell, the sugar is broken down through a series of reactions “the citric acid cycle”.  

PraxiLabs provides more than 50 biology virtual lab simulations that you can access anywhere and anytime.

  Subscribe and get started now!

About Nourhan Essam

' src=

Study Mind logo

Book a free consultation now

100+ Video Tutorials, Flashcards and Weekly Seminars

  • Revision notes >
  • A-Level Biology >
  • CIE A-level Biology

The Krebs Cycle (A-level Biology)

The krebs cycle.

A-level Biology - The Krebs Cycle

Each molecule of Acetyl-CoA formed during the link reaction enters the Krebs Cycle , which takes place in the mitochondrial matrix .

For every molecule of glucose that undergoes glycolysis, two Acetyl-CoA are made in the link reaction, and therefore two rounds of the Krebs Cycle occur (one for each molecule of acetyl-CoA).

Stages of Krebs Cycle

The following steps are in terms of 1 acetate molecule . But there will be two acetates per glucose molecule .

  • The acetate is released from CoA. CoA is used to transport acetate from the link reaction to the Krebs cycle. As soon as the Krebs cycle begins, acetate is unloaded.
  • Acetate joins with oxaloacetate. Acetate (2C) combines with oxaloacetate (4C), forming a 6C molecule called citrate .
  • Citrate is decarboxylated and dehydrogenated. Citrate (6C) loses a carboxyl group and forms a 5C molecule, releasing CO 2 in the process. It also loses two hydrogens, which are accepted by NAD to form reduced NAD .
  • The 5C molecule is decarboxylated and dehydrogenated. The 5C molecule is also decarboxylated and dehydrogenated , forming a 4C molecule. Again, NAD accepts the lost hydrogen, forming another reduced NAD .
  • The first 4C molecule is converted to a second 4C molecule . The 4C molecule undergoes a reaction, changing to another 4C molecule. In the process the original 4C molecule gives a phosphate group to ADP , leading to production of ATP . This is substrate-level phosphorylation , as the 4C compound (substrate) is phosphorylating ADP during the reaction.
  • The second 4C molecule is converted to a third 4C molecule. The second 4C is converted to another 4C molecule. Two hydrogens are released, and accepted by FAD, making reduced FAD .
  • The third 4C molecule is converted to oxaloacetate . The third 4C is dehydrogenated. This re-forms the oxaloacetate, completing the cycle. Another pair of hydrogen atoms are released, making reduced NAD .

A-level Biology - The Krebs Cycle

Products of Krebs Cycle

The reduced NAD and reduced FAD produced in the link reaction and Kreb Cycle are important for the final stage – oxidative phosphorylation .

Per molecule of glucose (and hence per 2 molecules of acetyl-CoA) Kreb’s cycle produces:

  • 2 ATP – some energy is produced in the form of ATP.
  • 6 reduced NAD – just like the reduced NAD from the previous two steps, the reduced NAD from the Krebs cycle goes to oxidative phosphorylation.
  • 2 reduced FAD – the reduced FAD joins reduced NAD in going to oxidative phosphorylation.
  • 1 coenzyme A – this goes back to the link reaction where it can be used to transport another acetate to the Krebs cycle.

The Krebs Cycle, also known as the citric acid cycle or the tricarboxylic acid cycle, is a series of chemical reactions that occur in cells to produce energy from the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins.

The main function of the Krebs Cycle is to produce energy in the form of ATP (adenosine triphosphate) through the oxidation of acetyl-CoA. The ATP produced by the Krebs Cycle can be used by the body for various functions, including muscle contraction and the transport of substances across cell membranes.

The main steps of the Krebs Cycle include the conversion of acetyl-CoA to citric acid, the series of chemical reactions that occur to produce energy, and the production of carbon dioxide as a waste product.

The Krebs Cycle interacts with other metabolic pathways, such as glycolysis and the electron transport chain, to produce energy for the body. The products of glycolysis are converted into acetyl-CoA, which then enters the Krebs Cycle, and the energy produced by the Krebs Cycle is used by the electron transport chain to produce ATP.

Enzymes play a crucial role in the Krebs Cycle by catalyzing the reactions that occur. They speed up the reactions and ensure that the Krebs Cycle runs smoothly and efficiently.

No, the Krebs Cycle cannot occur without oxygen. Oxygen is required to complete the electron transport chain and produce ATP, which is a key component of the Krebs Cycle.

If there is a deficiency in the enzymes involved in the Krebs Cycle, the reactions may not occur efficiently or at all. This can result in a buildup of toxic substances and a decreased ability of the body to produce energy, leading to a variety of health problems.

Still got a question? Leave a comment

Leave a comment, cancel reply.

Save my name, email, and website in this browser for the next time I comment.

CIE 1 Cell structure

Roles of atp (a-level biology), atp as an energy source (a-level biology), the synthesis and hydrolysis of atp (a-level biology), the structure of atp (a-level biology), magnification and resolution (a-level biology), calculating cell size (a-level biology), studying cells: confocal microscopes (a-level biology), studying cells: electron microscopes (a-level biology), studying cells: light microscopes (a-level biology), life cycle and replication of viruses (a-level biology), cie 10 infectious disease, bacteria, antibiotics, and other medicines (a-level biology), pathogens and infectious diseases (a-level biology), cie 11 immunity, types of immunity and vaccinations (a-level biology), structure and function of antibodies (a-level biology), the adaptive immune response (a-level biology), introduction to the immune system (a-level biology), primary defences against pathogens (a-level biology), cie 12 energy and respiration, anaerobic respiration in mammals, plants and fungi (a-level biology), anaerobic respiration (a-level biology), oxidative phosphorylation and chemiosmosis (a-level biology), oxidative phosphorylation and the electron transport chain (a-level biology), the link reaction (a-level biology), the stages and products of glycolysis (a-level biology), glycolysis (a-level biology), the structure of mitochondria (a-level biology), the need for cellular respiration (a-level biology), cie 13 photosynthesis, limiting factors of photosynthesis (a-level biology), cyclic and non-cyclic phosphorylation (a-level biology), the 2 stages of photosynthesis (a-level biology), photosystems and photosynthetic pigments (a-level biology), site of photosynthesis, overview of photosynthesis (a-level biology), cie 14 homeostasis, ectotherms and endotherms (a-level biology), thermoregulation (a-level biology), plant responses to changes in the environment (a-level biology), cie 15 control and co-ordination, the nervous system (a-level biology), sources of atp during contraction (a-level biology), the ultrastructure of the sarcomere during contraction (a-level biology), the role of troponin and tropomyosin (a-level biology), the structure of myofibrils (a-level biology), slow and fast twitch muscles (a-level biology), the structure of mammalian muscles (a-level biology), how muscles allow movement (a-level biology), the neuromuscular junction (a-level biology), features of synapses (a-level biology), cie 16 inherited change, calculating genetic diversity (a-level biology), how meiosis produces variation (a-level biology), cell division by meiosis (a-level biology), importance of meiosis (a-level biology), cie 17 selection and evolution, types of selection (a-level biology), mechanism of natural selection (a-level biology), types of variation (a-level biology), cie 18 biodiversity, classification and conservation, biodiversity and gene technology (a-level biology), factors affecting biodiversity (a-level biology), biodiversity calculations (a-level biology), introducing biodiversity (a-level biology), the three domain system (a-level biology), phylogeny and classification (a-level biology), classifying organisms (a-level biology), cie 19 genetic technology, cie 2 biological molecules, properties of water (a-level biology), structure of water (a-level biology), test for lipids and proteins (a-level biology), tests for carbohydrates (a-level biology), protein structures: globular and fibrous proteins (a-level biology), protein structures: tertiary and quaternary structures (a-level biology), protein structures: primary and secondary structures (a-level biology), protein formation (a-level biology), proteins and amino acids: an introduction (a-level biology), phospholipid bilayer (a-level biology), cie 3 enzymes, enzymes: inhibitors (a-level biology), enzymes: rates of reaction (a-level biology), enzymes: intracellular and extracellular forms (a-level biology), enzymes: mechanism of action (a-level biology), enzymes: key concepts (a-level biology), enzymes: introduction (a-level biology), cie 4 cell membranes and transport, transport across membranes: active transport (a-level biology), investigating transport across membranes (a-level biology), transport across membranes: osmosis (a-level biology), transport across membranes: diffusion (a-level biology), signalling across cell membranes (a-level biology), function of cell membrane (a-level biology), factors affecting cell membrane structure (a-level biology), structure of cell membranes (a-level biology), cie 5 the mitotic cell cycle, chromosome mutations (a-level biology), cell division: checkpoints and mutations (a-level biology), cell division: phases of mitosis (a-level biology), cell division: the cell cycle (a-level biology), cell division: chromosomes (a-level biology), cie 6 nucleic acids and protein synthesis, transfer rna (a-level biology), transcription (a-level biology), messenger rna (a-level biology), introducing the genetic code (a-level biology), genes and protein synthesis (a-level biology), synthesising proteins from dna (a-level biology), structure of rna (a-level biology), dna replication (a-level biology), dna structure and the double helix (a-level biology), polynucleotides (a-level biology), cie 7 transport in plants, translocation and evidence of the mass flow hypothesis (a-level biology), the phloem (a-level biology), importance of and evidence for transpiration (a-level biology), introduction to transpiration (a-level biology), the pathway and movement of water into the roots and xylem (a-level biology), the xylem (a-level biology), cie 8 transport in mammals, controlling heart rate (a-level biology), structure of the heart (a-level biology), transport of carbon dioxide (a-level biology), transport of oxygen (a-level biology), exchange in capillaries (a-level biology), structure and function of blood vessels (a-level biology), cie 9 gas exchange and smoking, lung disease (a-level biology), pulmonary ventilation rate (a-level biology), ventilation (a-level biology), structure of the lungs (a-level biology), general features of exchange surfaces (a-level biology), understanding surface area to volume ratio (a-level biology), the need for exchange surfaces (a-level biology), edexcel a 1: lifestyle, health and risk, phospholipids – introduction (a-level biology), edexcel a 2: genes and health, features of the genetic code (a-level biology), gas exchange in plants (a-level biology), gas exchange in insects (a-level biology), edexcel a 3: voice of the genome, edexcel a 4: biodiversity and natural resources, edexcel a 5: on the wild side, reducing biomass loss (a-level biology), sources of biomass loss (a-level biology), transfer of biomass (a-level biology), measuring biomass (a-level biology), net primary production (a-level biology), gross primary production (a-level biology), trophic levels (a-level biology), edexcel a 6: immunity, infection & forensics, microbial techniques (a-level biology), the innate immune response (a-level biology), edexcel a 7: run for your life, edexcel a 8: grey matter, inhibitory synapses (a-level biology), synaptic transmission (a-level biology), the structure of the synapse (a-level biology), factors affecting the speed of transmission (a-level biology), myelination (a-level biology), the refractory period (a-level biology), all or nothing principle (a-level biology), edexcel b 1: biological molecules, inorganic ions (a-level biology), edexcel b 10: ecosystems, nitrogen cycle: nitrification and denitrification (a-level biology), the phosphorus cycle (a-level biology), nitrogen cycle: fixation and ammonification (a-level biology), introduction to nutrient cycles (a-level biology), edexcel b 2: cells, viruses, reproduction, edexcel b 3: classification & biodiversity, edexcel b 4: exchange and transport, edexcel b 5: energy for biological processes, edexcel b 6: microbiology and pathogens, edexcel b 7: modern genetics, edexcel b 8: origins of genetic variation, edexcel b 9: control systems, ocr 2.1.1 cell structure, structure of prokaryotic cells (a-level biology), eukaryotic cells: comparing plant and animal cells (a-level biology), eukaryotic cells: plant cell organelles (a-level biology), eukaryotic cells: the endoplasmic reticulum (a-level biology), eukaryotic cells: the golgi apparatus and lysosomes (a-level biology), ocr 2.1.2 biological molecules, introduction to eukaryotic cells and organelles (a-level biology), ocr 2.1.3 nucleotides and nucleic acids, ocr 2.1.4 enzymes, ocr 2.1.5 biological membranes, ocr 2.1.6 cell division, diversity & organisation, ocr 3.1.1 exchange surfaces, ocr 3.1.2 transport in animals, ocr 3.1.3 transport in plants, examples of xerophytes (a-level biology), introduction to xerophytes (a-level biology), ocr 4.1.1 communicable diseases, structure of viruses (a-level biology), ocr 4.2.1 biodiversity, ocr 4.2.2 classification and evolution, ocr 5.1.1 communication and homeostasis, the resting potential (a-level biology), ocr 5.1.2 excretion, ocr 5.1.3 neuronal communication, hyperpolarisation and transmission of the action potential (a-level biology), depolarisation and repolarisation in the action potential (a-level biology), ocr 5.1.4 hormonal communication, ocr 5.1.5 plant and animal responses, ocr 5.2.1 photosynthesis, ocr 5.2.2 respiration, ocr 6.1.1 cellular control, ocr 6.1.2 patterns of inheritance, ocr 6.1.3 manipulating genomes, ocr 6.2.1 cloning and biotechnology, ocr 6.3.1 ecosystems, ocr 6.3.2 populations and sustainability.

assignment on krebs cycle

Let's get acquainted ? What is your name?

Nice to meet you, {{name}} what is your preferred e-mail address, nice to meet you, {{name}} what is your preferred phone number, what is your preferred phone number, just to check, what are you interested in, when should we call you.

It would be great to have a 15m chat to discuss a personalised plan and answer any questions

What time works best for you? (UK Time)

Pick a time-slot that works best for you ?

How many hours of 1-1 tutoring are you looking for?

My whatsapp number is..., for our safeguarding policy, please confirm....

Please provide the mobile number of a guardian/parent

Which online course are you interested in?

What is your query, you can apply for a bursary by clicking this link, sure, what is your query, thank you for your response. we will aim to get back to you within 12-24 hours., lock in a 2 hour 1-1 tutoring lesson now.

If you're ready and keen to get started click the button below to book your first 2 hour 1-1 tutoring lesson with us. Connect with a tutor from a university of your choice in minutes. (Use FAST5 to get 5% Off!)

Logo for Open Educational Resources

24.4 Protein Metabolism

Learning objectives.

By the end of this section, you will be able to:

  • Describe how, when, and why the body metabolizes proteins
  • Describe how the body digests proteins
  • Explain how the urea cycle prevents toxic concentrations of nitrogen
  • Differentiate between glucogenic and ketogenic amino acids
  • Explain how protein can be used for energy

Much of the body is made of protein, and these proteins take on a myriad of forms. They represent cell signaling receptors, signaling molecules, structural members, enzymes, intracellular trafficking components, extracellular matrix scaffolds, ion pumps, ion channels, oxygen and CO 2 transporters (hemoglobin). That is not even the complete list! There is protein in bones (collagen), muscles, and tendons; the hemoglobin that transports oxygen; and enzymes that catalyze all biochemical reactions. Protein is also used for growth and repair. Amid all these necessary functions, proteins also hold the potential to serve as a metabolic fuel source. Proteins are not stored for later use, so excess proteins must be converted into glucose or triglycerides, and used to supply energy or build energy reserves. Although the body can synthesize proteins from amino acids, food is an important source of those amino acids, especially because humans cannot synthesize all of the 20 amino acids used to build proteins.

The digestion of proteins begins in the stomach. When protein-rich foods enter the stomach, they are greeted by a mixture of the enzyme pepsin and hydrochloric acid (HCl; 0.5 percent). The latter produces an environmental pH of 1.5–3.5 that denatures proteins within food. Pepsin cuts proteins into smaller polypeptides and their constituent amino acids. When the food-gastric juice mixture (chyme) enters the small intestine, the pancreas releases sodium bicarbonate to neutralize the HCl. This helps to protect the lining of the intestine. The small intestine also releases digestive hormones, including secretin and CCK, which stimulate digestive processes to break down the proteins further. Secretin also stimulates the pancreas to release sodium bicarbonate. The pancreas releases most of the digestive enzymes, including the proteases trypsin, chymotrypsin, carboxypeptidase, and elastase , which aid protein digestion. Together, all of these enzymes break complex proteins into smaller individual amino acids ( Figure 24.4.1 ), which are then transported across the intestinal mucosa to be used to create new proteins, or to be converted into fats or acetyl CoA and used in the Krebs cycle.

The left panel shows the main organs of the digestive system, and the right panel shows a magnified view of the intestine. Text callouts indicate the different protein digesting enzymes produced in different organs.

In order to avoid breaking down the proteins that make up the pancreas and small intestine, pancreatic enzymes are released as inactive proenzymes that are only activated in the small intestine. In the pancreas, vesicles store trypsin, chymotrypsin, and carboxypeptidase as trypsinogen , chymotrypsinogen, and procarboxypeptidase . Once released into the small intestine, an enzyme found in the wall of the small intestine, called enterokinase , binds to trypsinogen and converts it into its active form, trypsin. Trypsin then binds to chymotrypsinogen and procarboxypeptidase to convert it into the active chymotrypsin and carboxypeptidase. Trypsin, chymotrypsin, and carboxypeptidase break down large proteins into smaller peptides, a process called proteolysis . These smaller peptides are catabolized into their constituent amino acids by the brush border enzymes, aminopeptidase and dipeptidase.  The free amino acids are then transported across the apical surface of the intestinal mucosa in a process that is mediated by secondary active transport using sodium-amino acid transporters. These transporters bind sodium and then bind the amino acid to transport it across the membrane. At the basal surface of the mucosal cells, the sodium and amino acid are released. The sodium can be reused in the transporter, whereas the amino acids are transferred into the bloodstream to be transported to the liver and cells throughout the body for protein synthesis.

Freely available amino acids are used to create proteins. If amino acids exist in excess, the body has no capacity or mechanism for their storage; thus, they are converted into glucose or ketones, or they are decomposed. Amino acid decomposition results in hydrocarbons and nitrogenous waste. However, high concentrations of nitrogen are toxic as they produce ammonium ions. The urea cycle processes nitrogen and facilitates its excretion from the body.

The urea cycle is a set of biochemical reactions that produces urea from ammonium ions in order to prevent a toxic level of ammonium in the body. It occurs primarily in the liver and, to a lesser extent, in the kidney. Prior to the urea cycle, ammonium ions are produced from the breakdown of amino acids. In these reactions, an amine group, or ammonium ion, from the amino acid is exchanged with a keto group on another molecule. This transamination event creates a molecule that is necessary for the Krebs cycle and an ammonium ion that enters into the urea cycle to be eliminated.

In the urea cycle, ammonium is combined with CO 2 , resulting in urea and water. The urea is eliminated through the kidneys in the urine ( Figure 24.4.2 ).

This image shows the reactions of the urea cycle and the organelles in which they take place.

Amino acids can also be used as a source of energy, especially in times of starvation. Because the processing of amino acids results in the creation of metabolic intermediates, including pyruvate, acetyl CoA, acetoacyl CoA, oxaloacetate, and α-ketoglutarate, amino acids can serve as a source of energy production through the Krebs cycle ( Figure 24.4.3 ). Figure 24.4.4 summarizes the pathways of catabolism and anabolism for carbohydrates, lipids, and proteins.

This figure shows the different reactions in which products of carbohydrate breakdown are converted into different amino acids.

Pyruvate dehydrogenase complex deficiency (PDCD) and phenylketonuria (PKU) are genetic disorders. Pyruvate dehydrogenase is the enzyme that converts pyruvate into acetyl CoA, the molecule necessary to begin the Krebs cycle to produce ATP. With low levels of the pyruvate dehydrogenase complex (PDC), the rate of cycling through the Krebs cycle is dramatically reduced. This results in a decrease in the total amount of energy that is produced by the cells of the body. PDC deficiency results in a neurodegenerative disease that ranges in severity, depending on the levels of the PDC enzyme. It may cause developmental defects, muscle spasms, and death. Treatments can include diet modification, vitamin supplementation, and gene therapy; however, damage to the central nervous system usually cannot be reversed.

PKU affects about 1 in every 15,000 births in the United States. People afflicted with PKU lack sufficient activity of the enzyme phenylalanine hydroxylase and are therefore unable to break down phenylalanine into tyrosine adequately. Because of this, levels of phenylalanine rise to toxic levels in the body, which results in damage to the central nervous system and brain. Symptoms include delayed neurological development, hyperactivity, mental retardation, seizures, skin rash, tremors, and uncontrolled movements of the arms and legs. Pregnant women with PKU are at a high risk for exposing the fetus to too much phenylalanine, which can cross the placenta and affect fetal development. Babies exposed to excess phenylalanine in utero may present with heart defects, physical and/or mental retardation, and microcephaly. Every infant in the United States and Canada is tested at birth to determine whether PKU is present. The earlier a modified diet is begun, the less severe the symptoms will be. The person must closely follow a strict diet that is low in phenylalanine to avoid symptoms and damage. Phenylalanine is found in high concentrations in artificial sweeteners, including aspartame. Therefore, these sweeteners must be avoided. Some animal products and certain starches are also high in phenylalanine, and intake of these foods should be carefully monitored.

Chapter Review

Digestion of proteins begins in the stomach, where HCl and pepsin begin the process of breaking down proteins into their constituent amino acids. As the chyme enters the small intestine, it mixes with bicarbonate and digestive enzymes. The bicarbonate neutralizes the acidic HCl, and the digestive enzymes break down the proteins into smaller peptides and amino acids. Digestive hormones secretin and CCK are released from the small intestine to aid in digestive processes, and digestive proenzymes are released from the pancreas (trypsinogen and chymotrypsinogen). Enterokinase, an enzyme located in the wall of the small intestine, activates trypsin, which in turn activates chymotrypsin. These enzymes liberate the individual amino acids that are then transported via sodium-amino acid transporters across the intestinal wall into the cell. The amino acids are then transported into the bloodstream for dispersal to the liver and cells throughout the body to be used to create new proteins. When in excess, the amino acids are processed and stored as glucose or ketones. The nitrogen waste that is liberated in this process is converted to urea in the urea acid cycle and eliminated in the urine. In times of starvation, amino acids can be used as an energy source and processed through the Krebs cycle.

Review Questions

Critical thinking questions.

1. Amino acids are not stored in the body. Describe how excess amino acids are processed in the cell.

2. Release of trypsin and chymotrypsin in their active form can result in the digestion of the pancreas or small intestine itself. What mechanism does the body employ to prevent its self-destruction?

Answers for Critical Thinking Questions

  • Amino acids are not stored in the body. The individual amino acids are broken down into pyruvate, acetyl CoA, or intermediates of the Krebs cycle, and used for energy or for lipogenesis reactions to be stored as fats.
  • Trypsin and chymotrypsin are released as inactive proenzymes. They are only activated in the small intestine, where they act upon ingested proteins in the food. This helps avoid unintended breakdown of the pancreas or small intestine.

This work, Anatomy & Physiology, is adapted from Anatomy & Physiology by OpenStax , licensed under CC BY . This edition, with revised content and artwork, is licensed under CC BY-SA except where otherwise noted.

Images, from Anatomy & Physiology by OpenStax , are licensed under CC BY except where otherwise noted.

Access the original for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction .

Anatomy & Physiology Copyright © 2019 by Lindsay M. Biga, Staci Bronson, Sierra Dawson, Amy Harwell, Robin Hopkins, Joel Kaufmann, Mike LeMaster, Philip Matern, Katie Morrison-Graham, Kristen Oja, Devon Quick, Jon Runyeon, OSU OERU, and OpenStax is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License , except where otherwise noted.

Share This Book

Presentation on Kreb’s Cycle

Basic objective of this lecture is to Presentation on Kreb’s Cycle. This presentation focus to discuss on Makes ATP, Makes NADH and Makes FADH2. Here also analysis Requires some carbohydrate to run and Watch for reaction coupling. This lecture also focus on Glycolysis in the cytosol and Krebs in mitochondrial matrix. Finally analysis on Aconitase Reaction, Isocitrate Dehydrogenase, Succinate dehydrogenase and Succinyl CoA synthetase. All these are include in Kreb’s Cycle, all process are explain with examples.

Lecture on Organic Chemistry

Presentation on nuclear reactions, chloromonoxide, relative mass formula, atomic mass and empirical formula, mortgage bank, insolvency definition, the significance of light for the variety of grassland plants, term paper on financial system of pran group, presentation on citizenship quotes, ammonium carbonate, latest post, construction management (cm), earth shelter, embodied music cognition, motor cognition, zebrafish navigates to find their suitable temperature, the new evolutionary theory explains why creatures shrink with time.

IMAGES

  1. Assignment 5

    assignment on krebs cycle

  2. Assignment 5

    assignment on krebs cycle

  3. Krebs Cycle

    assignment on krebs cycle

  4. Biosynthesis

    assignment on krebs cycle

  5. Biochemistry: kreb cycle steps and regulation

    assignment on krebs cycle

  6. Pin on MyAssignmentHelp

    assignment on krebs cycle

VIDEO

  1. Krebs cycle

  2. KREBS CYCLE MADE EASY

  3. Krebs cycle trick made easy

  4. The Krebs Cycle Explained (Aerobic Respiration)

  5. Krebs Cycle Explained!

  6. KREBS CYCLE MADE SIMPLE

COMMENTS

  1. PDF The Krebs Cycle

    One atom is removed via and is removed using . becomes attached to the remaining atoms, creating , which then enters the Krebs cycle. Krebs Cycle enters the cycle and then combines CoA CoA-SH CoA-SH CoA-SH Products of the Krebs Cycle with to make the six-carbon compound .

  2. 10.1: The Krebs Cycle (Citric Acid Cycle)

    In prokaryotic cells, the citric acid cycle occurs in the cytoplasm; in eukaryotic cells the citric acid cycle takes place in the matrix of the mitochondria. The overall reaction for the citric acid cycle is: 2 acetyl groups + 6 NAD++2 FAD+2 ADP+2 Pi → 4 CO2 + 6 NADH + 6H++2 FADH2 + 2 ATP. Figure 10.1: The citric acid cycle.

  3. The citric acid cycle

    The cycle includes eight major steps. Simplified diagram of the citric acid cycle. First, acetyl CoA combines with oxaloacetate, a four-carbon molecule, losing the CoA group and forming the six-carbon molecule citrate.

  4. Krebs Cycle

    Reviewed by: BD Editors Last Updated: January 15, 2021 Krebs Cycle Definition The Krebs Cycle, also called the citric acid cycle, is the second major step in oxidative phosphorylation.

  5. Krebs / citric acid cycle (video)

    12 years ago Near the end of the video, it says at the end of cellular respiration you end up with the promised 38 ATPs. My textbook says "The complete breakdown of glucose through cellular respiration, including glycolysis, results in the production of 36 molecules of ATP. Where did the extra 2 ATPs go? • 2 comments ( 21 votes) Upvote Flag

  6. 2.28: Krebs Cycle

    Before the Krebs cycle begins, pyruvic acid, which has three carbon atoms, is split apart and combined with an enzyme known as CoA, which stands for coenzyme A. The product of this reaction is a two-carbon molecule called acetyl-CoA. The third carbon from pyruvic acid combines with oxygen to form carbon dioxide, which is released as a waste ...

  7. The Krebs Cycle

    The Krebs cycle is also known as the Citric Acid Cycle or the tricarboxylic acid cycle (TCA cycle). Within the mitochondria, each pyruvate is broken apart and combined with a coenzyme known as CoA to form a 2-carbon molecule, Acetyl-CoA, which can enter the Krebs Cycle. A single atom of carbon (per pyruvate) is "lost" as carbon dioxide.

  8. Physiology, Krebs Cycle

    The Krebs cycle, also known as the citric acid cycle or the tricarboxylic acid cycle, is a key metabolic pathway that occurs in the mitochondria of living cells. It involves the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins into carbon dioxide and chemical energy. This book chapter from the National Center for Biotechnology Information provides an overview of the ...

  9. 6.6: The Krebs/TCA/Citric acid cycle

    The Krebs cycle is the first pathway of oxygenic respiration. Evolution of this respiration and the chemical bridge from glycolysis to the Krebs cycle, no doubt occurred a few reactions at a time, perhaps at first as a means of protecting anaerobic cells from the 'poisonous' effects of oxygen. Later, natural selection fleshed out the ...

  10. The TCA Cycle

    The TCA cycle is a central pathway that provides a unifying point for many metabolites, which feed into it at various points. It takes place over eight different steps: Step 1: Acetyl CoA (two-carbon molecule) joins with oxaloacetate (four-carbon molecule) to form citrate (six-carbon molecule).

  11. The Krebs Cycle Made Easy

    The Krebs cycle, named after 1953 Nobel Prize winner and physiologist Hans Krebs, is a series of metabolic reactions that take place in the mitochondria of eukaryotic cells.Put more simply, this means that bacteria do not have the cellular machinery for the Krebs cycle, so it limited to plants, animals and fungi.

  12. Krebs Cycle ( Read )

    mins Krebs Cycle What will you learn The role of the Krebs cycle in cellular respiration What type of acid do these fruits contain? Citric acid. Citric acid is also the first product formed in the Krebs cycle, and therefore this acid occurs in the metabolism of virtually all living things. Cellular Respiration Stage II: The Krebs Cycle

  13. Krebs Cycle Study Guide (That Will Help You Actually Remember It)

    myMedStudy MedStudy makes learning medicine easier. From board prep to continuing ed, wherever you are in your medical journey, our study solutions can help you succeed. Follow our Krebs Cycle study guide using the MedStudy Method to remember it for the long term.

  14. Krebs Cycle

    Krebs Cycle or Citric Acid Cycle It is the common pathway for complete oxidation of carbohydrates, proteins, and lipids as they are metabolized to acetyl coenzyme A or other intermediates of the cycle. The Acetyl CoA produced enters the Tricarboxylic acid cycle or Citric acid cycle. Glucose is fully oxidized in this process.

  15. Krebs Cycle or Citric Acid Cycle: Steps, Products, Significance

    Introduction The Krebs cycle or TCA cycle (tricarboxylic acid cycle) or Citric acid cycle is a series of enzyme catalysed reactions occurring in the mitochondrial matrix, where acetyl-CoA is oxidised to form carbon dioxide and coenzymes are reduced, which generate ATP in the electron transport chain.

  16. The Krebs Cycle

    The Krebs cycle definition is a sequence of chemical reactions that occur in the body. The cycle starts with the intake of food, which is broken down into small molecules by the stomach and intestines. These molecules are then absorbed by the body through the small intestines and transported to the liver via the bloodstream.

  17. The Krebs Cycle (A-level Biology)

    The Krebs Cycle (A-level Biology) The Krebs Cycle . A-level Biology - The Krebs Cycle. Overview. Each molecule of Acetyl-CoA formed during the link reaction enters the Krebs Cycle, which takes place in the mitochondrial matrix.. For every molecule of glucose that undergoes glycolysis, two Acetyl-CoA are made in the link reaction, and therefore two rounds of the Krebs Cycle occur (one for ...

  18. 24.4 Protein Metabolism

    In the urea cycle, ammonium is combined with CO 2, resulting in urea and water. The urea is eliminated through the kidneys in the urine (Figure 24.4.2). Figure 24.4.2 - Urea Cycle: Nitrogen is transaminated, creating ammonia and intermediates of the Krebs cycle. Ammonia is processed in the urea cycle to produce urea that is eliminated through ...

  19. Krebs Cycle ( Read )

    Describes the steps and products of the Krebs Cycle, the second of three stages of cellular respiration. All Modalities. Add to Library. Details. Resources. Download. Quick Tips. Notes/Highlights. Vocabulary.

  20. 5.2.5 The Krebs Cycle

    The Krebs cycle (sometimes called the citric acid cycle) consists of a series of enzyme-controlled reactions. 2 carbon (2C) Acetyl CoA enters the circular pathway from the link reaction in glucose metabolism. Acetyl CoA formed from fatty acids (after the breakdown of lipids) and amino acids enters directly into the Krebs Cycle from other ...

  21. Krebs Cycle

    The "Krebs cycle" is a series of chemical reactions used by all aerobic organisms in their energy conversion processes. It is a series of enzymatic reactions that occur in all aerobic organisms; it involves the oxidative metabolism of acetyl units and serves as the main source of cellular energy. It is important to many biochemical pathways.

  22. Lecture on Krebs Cycle

    Lecture Krebs Cycle occurs in the matrix of the mitochondrion. Major purpose of this lecture is to present on Krebs Cycle. The Krebs Cycle is the central metabolic pathway in all aerobic organisms. Citric acid (6C) is gradually converted back to the 4-carbon compound - ready to start the cycle once more.

  23. Presentation on Kreb's Cycle

    Lecture Presentation. Basic objective of this lecture is to Presentation on Kreb's Cycle. This presentation focus to discuss on Makes ATP, Makes NADH and Makes FADH2. Here also analysis Requires some carbohydrate to run and Watch for reaction coupling. This lecture also focus on Glycolysis in the cytosol and Krebs in mitochondrial matrix.