In the Krebs cycle are the intermediates constantly oxidized by dehydrogenase enzymes? (in terms of conversion
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There is a delicate balance of Krebs Cycle intermediates, as different physiological conditions require different amounts of each one.  For example, if the body needs to make glucose (gluconeogenesis), it may remove oxaloacetate for this pathway.  Or if it is low for a specific amino acid, it may pull out certain Krebs Cycle intermediates to synthesize it, or it may use citrate to synthesize fatty acids. \n\nGenerally there is also reverse reactions that FILL UP Krebs Cycle intermediates.
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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.
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The first of the two key enzymes is unique to the ED pathway, 6-phosphogluconate dehydratase (Edd), which catalyzes a dehydration of 6-phosphogluconate to form KDPG. The second enzyme of the ED pathway, KDPG aldolase (Eda), catalyzes an aldol cleavage of KDPG to form pyruvate and glyceraldehyde-3-phosphate. The triose phosphate intermediate is further metabolized by the glycolytic pathway and provides energy via substrate-level phosphorylation.
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ATP from the Krebs Cycle making the proton gradient in the electron transport chain
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Look at your diagram of Kreb's Carboxylic Acid Cycle.\nPick out oxaloacetic acid.\nWhat does it do?\nWhere does it come from? Remember the process is a cycle.
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Aerobic glycolysis of glucose to pyruvate, requires two equivalents of ATP to activate the process, with the subsequent production of four equivalents of ATP and two equivalents of NADH. Thus, conversion of one mole of glucose to two moles of pyruvate is accompanied by the net production of two moles each of ATP and NADH. \n\nGlucose + 2 ADP + 2 NAD+ + 2 Pi -----> 2 Pyruvate + 2 ATP + 2 NADH + 2 H+\n\nThe NADH generated during glycolysis is used to fuel mitochondrial ATP synthesis via oxidative phosphorylation, producing either two or three equivalents of ATP depending upon whether the glycerol phosphate shuttle or the malate-aspartate shuttle is used to transport the electrons from cytoplasmic NADH into the mitochondria. The net yield from the oxidation of 1 mole of glucose to 2 moles of pyruvate is, therefore, either 6 or 8 moles of ATP. Complete oxidation of the 2 moles of pyruvate, through the TCA cycle, yeilds an additional 30 moles of ATP; the total yield, therefore being either 36 or 38 moles of ATP from the complete oxidation of 1 mole of glucose to CO2 and H2O. Got it?
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Adenosine TriPhospahte (ATP) and NADH2\n\nIn response to answer above: GTP is only created from tyrosine-kinase reactors and is not part of the krebs cycle
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Substrate-level: production of ATP molecules via transfer of a phosphate group from an intermediate high-energy substrate directly to ADP.\n\nOxidative: production of ATP molecules from the redox reactions of an electron transport chain\n\nGylcolysis and Krebs cycle use substrate-level phosphorylation.  Electron transport chain uses oxidative phosphorylation.\n\nAlso, check out the link for a complete explanation: http://www.csun.edu/~hcbio029/BIOL315/Substrate_vs_oxidative.pdf#search='substrate%20oxidative%20phosphorylation%20difference'
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The citric acid cycle is also called the tricarboxylic acid (TCA) cycle and the Krebs cycle. It is the final common catabolic pathway for the oxidation of fuel molecules. Two carbons enter the citric acid cycle as acetyl CoA and two carbons leave as CO2. In the course of the cycle, four oxidation-reduction reactions take place to yield reduction potential in the form of three molecules of NADH and one molecule of FADH2. A high energy phosphate bond (GTP) is also formed.
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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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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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Glucose is broken down into pyravate with a net gain of 2 ATP during glyclolysis, pryravate is broken down into CO2 and acetyl CoA.   acetyl CoA is oxidized in the kerbs cycle or citric acid cycle to for NADH, CO2, FADH2.  NADH passes electrons to the electron transport chain where the electron is passed along a chain of electron acceptors lossing energy each time.  The electron transport chain drives the H+ ions across the membrane of the mitochondria which ends up producing ATP.  Oxygen is the final electron acceptor.  I know thats a lot of info but its not close to all of it. I hope this helps
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The majority of fatty acids are metabolized using beta-oxidation. Essentially, a series of four enzymes oxidize the beta-carbon, shorting the fatty acid chain by two carbons. The electrons lost are transferred to electron carriers, and a molecule of acetyl-CoA is produced.\n\nOne round of beta-oxidation produces 1 QH2, 1 NADH, and 1 acetyl-CoA molecule. The citric acid cycle is used to convert the molecule of acetyl-CoA into 3 NADH, 1 QH2, and 1 GTP. Through oxidative phosphorylation:\n\n2 QH2 --> 4 ATP (2 per QH2)\n4 NADH --> 12 ATP (3 per NADH)\n1 GTP --> 1 ATP\n\nEach round of beta-oxidation shortens the fatty acid chain by two carbons and produces 17 ATP. Therefore, one molecule of palmitoleic acid, which contains 16 carbons, could undergo beta-oxidation 7 times and produce 131 molecules of ATP!\n\nPS The answer directly below mine is for one molecule of glucose... Not what you want. Lipids don't go through glycolysis. Acetyl-CoA also cannot enter gluconeogenesis in humans either because we lack the enzyme needed to enter the glyoxylate cycle.
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Cyanide binds better to cytochrome 3a than oxygen and this affects the electron transport chain.  The last step in the electron transport chain is the transfer of electrons to oxygen gas using the cytochrome protein.  Cyanide binding to the cytochrome locks the protein and prevents electron transfer out of cytochrome 3a.  This messes up the whole electron transport chain as everything gets backed up in the mitochondrial inner membrane, which is where the cytochrome and other electron transport proteins are located.  \n\nSo when the electron transport chain is backed up this prevents the reducing power created in glycolysis and the Krebs Cycle from being used.  The reducing power from those two processes is what is used to create most of the energy derived from respiration.  So without use of the electron transport chain, which does not work when cyanide is present, only 3 or 4 ATP are made per glucose in the respiration reactions.  With the electron transport chain, in the absence of cyanide, about 34 ATP total are made from the respiration reactions.  \n\nSo overall cyanide greatly reduces the efficiency of respiration by preventing the use of a critical respiration protein.  The presence of cyanide in a cell can cause cell death within minutes due to the extreme inefficiency at which the cell produces energy.
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C is false since NADH is produced during glycolysis as well as during the TCA cycle, unlike FADH2 which is prodcued only in the TCA cycle.  Remember TCA takes place in the mitochondria and glycolysis is in the cytosol.
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Step 1 - ATP is invested by adding a P to glucose\n          Step 2 - Glucose-6-P is convertedinto Fructose-6-P\nStep 3 - A second ATP is invested \nStep 4 - The 6 carbon molecule issplit into two three carbon molecules.\nStep 4.5 - Dihydroxyacetone -P is converted into 3-P-glyceraldehyde\nStep 6 - every subsequent step occurs 2xNADH is produced as another P is added\nStep 7 - (2) ATP is recovered\nStep 8 - The P is moved from the 3-carbon to the 2-carbon\nStep 9 - A structural change is made\nStep 10 - (2) ATP is recovered\nStep 11 - NADH is produced anda CO2 is produced\n2 pyruvate are made from the process