what is the main function of the krebs cycle?
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The Krebs cycle, also called the Citric Acid Cycle, is a method by which cells undergo aerobic cellular respiration.
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The answer is C.  Glucose + oxygen are metabolized through glycolysis, the krebs cycle and electron transport chain to produce a net gain of 38 ATP (energy) and produce H20 and CO2 as byproducts.
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in the cytosplam during glycosis\nin the mitochondrial matrix(cytoplasm) in the citiric acid cycle, kreb cycle, or TCA.
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Metabolism is the sum of all chemical reactions within the body.  the basics can be broken down into 2 groups.. Catabolism and anabolism.  Catabolism is the chemical processes that break down complex molecules to release energy.  Anabolism is the process to build up complex chemical compounds from simpler chemical compounds using stored energy.  \nIf your want to know more you should run a search on Krebs cycle, Glycolosis, lipid metabolism, and Protien Anabolism/Catabolism
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It is metabolism of the glucose energy by Reduction-Oxidisation (RedOx) reactions to be used in the electron transfer chain to produce Adeonsie Triphosphate (ATP) which is the basic energy unit that is used in cells.
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The citric acid cycle (also known as the tricarboxylic acid cycle, the TCA cycle, or the Krebs cycle) is a series of chemical reactions of central importance in all living cells that utilize oxygen as part of cellular respiration. In aerobic organisms, the citric acid cycle is part of a metabolic pathway involved in the chemical conversion of carbohydrates, fats and proteins into carbon dioxide and water to generate a form of usable energy. It is the second of three metabolic pathways that are involved in fuel molecule catabolism and ATP production, the other two being glycolysis and oxidative phosphorylation.  Check out the link below for more information.
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1. In fermentation, pyruvic acid molecules from the glycolysis cycle are turned into other chemical compounds, and a little bit of energy (only two ATP molecules per molecule of glucose – actually four are produced in glycolysis, but two are used up before it reaches this stage) is produced, IN THE ABSENCE OF OXYGEN!\n2. It takes place in the cytoplasm.\n3. all eukaryotes, to some degree\n4. wine, beer, cheese, medications...all are products of fermentation
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The Kidney's primary function is to remove waste material from the blood stream.  Oxygen is used by every cell in the body to help metabolize nutrients.
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do u mean the steps of cellular respiration? if so...\n1. glycolysis\n2. pyruvate oxidation\n3. krebs' cycle\n4. electron transport chain
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The pathway of glycolysis can be seen as consisting of 2 separate phases. The first is the chemical priming phase requiring energy in the form of ATP, and the second is considered the energy-yielding phase. In the first phase, 2 equivalents of ATP are used to convert glucose to fructose 1,6-bisphosphate (F1,6BP). In the second phase F1,6BP is degraded to pyruvate, with the production of 4 equivalents of ATP and 2 equivalents of NADH.
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Kreb cycle and glycolysis - is what I initially answered\n\nHowever, if it is a standard test/textbook question the questioner is asking, then the answer is probably going to be 2 different mechanisms/pathways. It probably is going to be AEROBIC and ANAEROBIC metabolism.
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Biological systems have enzymes (and a handful of other reagents) which will use O2 and sugar to make energy--specifically, hexokinase (HK), phosphoglucose isomerase (PGI), phosphofructokinase (PFK), aldolase, triose phosphate isomerase (TIM), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), phosphoglycerate kinase (PGK), phosphoglycerate mutase (PGM), endolase, and pyruvate kinase (PK).  The process undergone is called glycolysis.  The result is that glucose is consumed, making two pyruvate molecules (which in some systems can then enter the Citric Acid Cycle aka Kreb's Cycle) and ADP is turned into ATP, which is an energy source.\n\nAnd after memorizing this and subsequently forgeting all this useless detail some years ago, I nearly ralphed on my book reading this just now.  Bad memories.
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There are five main ways that enzyme activity is controlled in the cell.\n\nEnzyme production (transcription and translation of enzyme genes) can be enhanced or diminished by a cell in response to changes in the cell's environment. This form of gene regulation is called enzyme induction and inhibition. For example, bacteria may become resistant to antibiotics such as penicillin because enzymes called beta-lactamases are induced that hydrolyse the crucial beta-lactam ring within the penicillin molecule. Another example are enzymes in the liver called cytochrome P450 oxidases, which are important in drug metabolism. Induction or inhibition of these enzymes can cause drug interactions. \n\nEnzymes can be compartmentalized, with different metabolic pathways occurring in different cellular compartments. For example, fatty acids are synthesized by one set of enzymes in the cytosol, endoplasmic reticulum and the Golgi apparatus and used by a different set of enzymes as a source of energy in the mitochondrion, through β-oxidation.\n\nEnzymes can be regulated by inhibitors and activators. For example, the end product(s) of a metabolic pathway are often inhibitors for one of the first enzymes of the pathway (usually the first irreversible step, called committed step), thus regulating the amount of end product made by the pathways. Such a regulatory mechanism is called a negative feedback mechanism, because the amount of the end product produced is regulated by its own concentration. Negative feedback mechanism can effectively adjust the rate of synthesis of intermediate metabolites according to the demands of the cells. This helps allocate materials and energy economically, and prevents the manufacture of excess end products. Like other homeostatic devices, the control of enzymatic action helps to maintain a stable internal environment in living organisms. \n\nEnzymes can be regulated through post-translational modification. This can include phosphorylation, myristoylation and glycosylation. For example, in the response to insulin, the phosphorylation of multiple enzymes, including glycogen synthase, helps control the synthesis or degradation of glycogen and allows the cell to respond to changes in blood sugar. Another example of post-translational modification is the cleavage of the polypeptide chain. Chymotrypsin, a digestive protease, is produced in inactive form as chymotrypsinogen in the pancreas and transported in this form to the stomach where it is activated. This stops the enzyme from digesting the pancreas or other tissues before it enters the gut. This type of inactive precursor to an enzyme is known as a zymogen. \n\nSome enzymes may become activated when localized to a different environment (eg. from a reducing (cytoplasm) to an oxidising (periplasm) environment, high pH to low pH etc). For example, hemagglutinin of the influenza virus undergoes a conformational change once it encounters the acidic environment of the host cell vesicle causing its activation.
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Oxidative phosphorylation is the terminal process of cellular respiration in eukaryotes. During oxidative phosphorylation electrons are transferred from NADH or FADH2 — created in glycolysis, fatty acid metabolism and the Krebs cycle — to molecular oxygen, via a series of protein complexes located in the inner mitochondrial membrane. Protons are pumped from the mitochondrial matrix into the intermembrane space as a result of this flow of electrons. This generates a pH gradient and a transmembrane electrical potential across the membrane. This is a form of potential energy which is referred to as a proton-motive force. The protons flow back into the mitochondrial matrix via a large protein complex, ATP synthase. This is how most of the ATP is created in a eukaryotic cell. This is the reaction that ATP synthase catalyses:\n\n\n\n\nADP3- + H+ + Pi ↔ ATP4- + H2O \n\nThe synthase functions almost as a mechanical motor, with each NADH molecule contributing enough proton motive force to generate 2.5 ATP. Each FADH2 molecule is worth 1.5 ATP. All together, the 10 NADH and 2 FADH2 molecules contributed through oxidation of glucose (glycolysis, conversion of pyruvate to acetyl-CoA, and the Krebs cycle) account for 23 of the 30 total ATP energy carrier molecules. It is worth noting that these ATP values are maximum values and in reality protons leak across the membrane causing somewhat lower values.\n\nPhotophosphorylation, which occurs when plants synthesize glucose during photosynthesis, also uses ATP synthase and a proton gradient to generate ATP. The process occurs across the thylakoid membrane when chlorophyll is energized by light and donates an excited electron to an electron transport chain.\n\nContents [hide]\n1 Inhibitors \n2 See also \n3 External links \n4 References \n \n\n\n[edit] Inhibitors\nThere are a few well-known toxins that affect the process of oxidative phosphorylation and can lead to breakdown of the chain:\n\nCyanide interrupts the electron transport chain in the inner membrane of the mitochondrion because it binds more strongly than oxygen to the Fe3+ (ferric iron ion) in cytochrome a3, preventing this cytochrome from combining electrons with oxygen. \nOligomycin functions by inhibiting the ATP synthase protein and preventing it from generating ATP from the proton gradient. \nCCCP (m-chloro-carbonylcyanide-phenylhydrazine) destroys the proton gradient by allowing the protons to flow out of the membrane. Without the gradient, the ATP synthase cannot function and ATP synthesis breaks down. \nA detergent, or substance that destroys cellular membranes by breaking apart their lipid bilayers, will destroy the membrane used in the process and prevent a proton gradient. \nRotenone prevents the transfer of electrons from Fe-S centers in Complex I (most notably) to ubiquinone. The electrons entering into Complex I are those derived from NADH, and provide the bulk of the reducing potential to the electron transport chain. \nFor each of these toxins, a backup will cause everything before it to break down as well. For example, if oligomycin is added, protons cannot pass through. As a result, the H+ pumps are unable to pass protons through because the gradient becomes too strong for them to overcome. NADH and FADH2 are then not oxidized and the citric acid cycle ceases to operate because there are no NAD+ and FAD coenzymes to be reduced.
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Oxidative phosphorylation is a biochemical process in cells. It is the final metabolic pathway of cellular respiration, after glycolysis and the citric acid cycle.\n\nPlease see the wikipedia article below for a detailed explanation:
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The answer is C.  Six molecule of 3-phosphoglycerate is produced per turn of the Calvin cycle (in the first step).  One full turn of the Calvin cycle requires the fixation of three CO2 molecules.  Also ATP and NADPH is used in the Calvin cycle and both are oxidized to lower energy forms.  Only 1 RuBP is produced per cycle.
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Glycolysis -- Cytoplasm\nKrebs Cycle(TCA) -- Matrix\nETS -- INNER membrane \nThe Krebs cycle, also called the citric acid cycle, is a fundamental metabolic pathway involving eight enzymes essential for energy production through aerobic respiration, and, like glycolysis, arose early in evolution. This pathway is also an important source of biosynthetic building blocks used in gluconeogenesis, amino acid biosynthesis, and fatty acid biosynthesis. The Krebs cycle takes place in mitochondria where it oxidizes acetyl-CoA, releasing carbon dioxide and extracting energy primarily as the reduced high-energy electron carriers NADH and FADH2. NADH and FADH2 transfer chemical energy from metabolic intermediates to the electron transport chain to create a different form of energy, a gradient of protons across the inner mitochondrial membrane. The energy of the proton gradient in turn drives synthesis of the high-energy phosphate bonds in ATP, the common energy currency of the cell used to drive a huge variety of reactions and processes. An acetyl-CoA molecule (2 carbons) enters the cycle when citrate synthase condenses it with oxaloacetate (4 carbons) to create citrate (6 carbons). One source of the acetyl-CoA that enters the Krebs cycle is the conversion of pyruvate from glycolysis to acetyl-CoA by pyruvate dehydrogenase. Acetyl-CoA is a key metabolic junction, derived not only from glycolysis but also from the oxidation of fatty acids.