citric acid cycle

Fluoroacetate can be converted to fluorocitrate, which is an inhibitor of aconitase. Arsenic is not a direct inhibitor, but arsenite is an inhibitor of lipoic acid–containing enzymes such as α-ketoglutarate dehydrogenase. Malonate, not malic acid, is an inhibitor of succinate dehydrogenase. The citric acid cycle requires oxygen and would be inhibited by anaerobic, not aerobic, conditions. Fluorouracil is a suicide inhibitor of thymidylate synthase and blocks deoxythymidylate synthesis. 

C i.e. ATP

The in vivo control of the TCA cycle is done by ATP and NADH.

Alanine-pyruvate aminotransferase (alanine aminotransferase) and glutamate-α-ketoglutarate aminotransferase (glutamate aminotransferase) catalyze the transfer of amino groups to pyruvate (forming alanine) or to α-ketoglutarate (forming glutamate).

Ammonia may be toxic to the brain in part because it reacts with α-ketoglutarate to form glutamate. The resulting depletion of α-ketoglutarate then impairs the function of the tricarboxylic acid (TCA) cycle in neurons.

Malonate competitively inhibits succinate dehydrogenase, which converts succinate to fumarate

Ans. is ‘c’ i.e., isoleucine

Amino acids that are catabolized to succinyl-CoA. Methionine, valine, and isoleucine are catabolized into propoinyl-CoA that is converted into d-methylmalonyl-CoA by propionyl-CoA carboxylase via fatty acids β-oxidation.

Acetyl CoA is a starting molecule, not an intermediate product of the citric acid cycle.

Ans. is ‘b’ i.e., Succinate thiokinase