Citric acid cycle result

One turn of the citric acid cycle results in how many ATP/ GTP ... 

One turn of the citric acid cycle results in the production of two CO2 molecules, three NADH molecules, one FADH2 molecule, and one ATP molecule. Oxidative phosphorylation yields three ATP molecules per NADH molecule and two ATP molecules per FADH2 molecule. The only exception to these energy yields is the NADH produced in the cytoplasm during glycolysis. Oxidative phosphorylation )delds only two ATP molecules per cytoplasmic NADH molecule. The reason for this is that energy must be expended to shuttle electrons from NADH in the cytoplasm to FADHj in the mitochondrion. 

The oxidation of pyruvate by the pyruvate dehydrogenase complex and the citric acid cycle results in the production of three molecules of COg. As a result of these oxidation reactions, one molecule of GDP is phosphorylated to GTP,... 

The initial stages of catabolism result in the conversion of both fats and carbohydrates into acetyl groups that are bonded through a thioester link to coenzyme A. Acetyl CoA then enters the next stage of catabolism—the citric acid cycle, also called the tricarboxylic acid (TCA) cycle, or Krebs tycle, after Hans Krebs, who unraveled its complexities in 1937. The overall result of the cycle is the conversion of an acetyl group into two molecules of C02 plus reduced coenzymes by the eight-step sequence of reactions shown in Figure 29.12. 

Figure 29.12 MECHANISM The citric acid cycle is an eight-step series of reactions that results in the conversion of an acetyl group into two molecules of C02 plus reduced coenzymes. Individual steps are explained in the text.

The final step is the oxidation of (S)-malate by NAD+ to give oxaloacetate, a reaction catalyzed by malate dehydrogenase. The citric acid cycle has now returned to its starting point, ready to revolve again. The overall result of the cycle is... 

Step 2 of Figure 29.13 Decarboxylation and Phosphorylation Decarboxylation of oxaloacetate, a jB-keto acid, occurs by the typical retro-aldol mechanism like that in step 3 in the citric acid cycle (Figure 29.12), and phosphorylation of the resultant pyruvate enolate ion by GTP occurs concurrently to give phosphoenol-pyruvate. The reaction is catalyzed by phosphoenolpyruvate carboxykinase. 

As a result of oxidations catalyzed by the dehydrogenases of the citric acid cycle, three molecules of NADH and one of FADHj are produced for each molecule of acetyl-CoA catabohzed in one mrn of the cycle. These reducing equivalents are transferred to the respiratory chain (Figure 16-2), where reoxidation of each NADH results in formation of 3 ATP and reoxidation of FADHj in formation of 2 ATP. In addition, 1 ATP (or GTP) is formed by substrate-level phosphorylation catalyzed by succinate thiokinase. 

Chenoweth believes that an explanation of the above results may lie in the reactions occurring before the entrance of fatty acid metabolites into the citric acid cycle. Activated acetate, i.e. acetyl coenzyme A (AcCoA) is the end-product of fatty acid metabolism prior to its condensation with oxalacetate to form citrate. Possibly fluoro-fatty acids behave like non-fluorinated fatty acids. The end-product before the oxalacetate condensation could be the same for all three fluorinated inhibitors, viz. fluoroacetyl coenzyme A (FAcCoA). Fluorocitrate could then be formed by the condensation of oxalacetate with FAcCoA, thereby blocking the citric acid cycle. The specificity of antagonisms must therefore occur before entrance of the metabolites into the citric acid cycle. 

Pitfalls associated with metabolic screening are numerous. They can result from proximal tubulopathy, causing a reduction in blood lactate and an increase in urinary lactate from diabetes mellitus, hampering entry of pyruvate into the citric acid cycle from tissue-specific involvement or partial deficiency, which may barely alter the redox status in plasma. When metabolic tests are negative, respiratory chain deficiency may be misdiagnosed. 

The result of this is that the pH difference and therefore potential difference across the membrane collapses, and there is no energy to drive the ATP synthesis. However, electrons can still flow through the chain, which drives the citric acid cycle to produce them, and so cellular metabolism still continues, and indeed, without the constraint of ATP synthesis, the electron flow is more rapid and so other metabolic rates also increase in rate. Oxygen can still be reduced to water, and so this will be used up also and require replacement. 

In mammals, high concentrations of fats in the diet result in increased synthesis of the enzymes of peroxisomal /3 oxidation in the liver. Liver peroxisomes do not contain the enzymes of the citric acid cycle and cannot catalyze the oxidation of acetyl-CoA to C02. Instead,... 

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