One of the enzymes that constitute the CAC (Citric Acid Cycle) is succinate dehydrogenase. This paper explores a hypothetical CAC when succinate dehydrogenase is defective (Kay & Weitzman, 1987).A defect in the enzyme inhibits the formation of fumarate along with ubiquinol. A defect in succinate dehydrogenase impacts on the rest of the CAC since the consequent substrates or products are successive derivatives of fumarate: L-malate, oxaloacetate, and citrate (McArdle, Katch & Katch, 2010). These products will not continue being made and the chain will stop.
The defect will affect the ETC (Electron Transport Chain) action. Usually, in CAC, electrons are succinate oxidation derivatives (Kay & Weitzman, 1987).Their derivation from the oxidation happens through FAD. The electrons tunnel down the Fe-S relay to the 3Fe-4S group. Subsequently, the electrons get transferred to an active site, specifically to a molecule of ubuquinone. The defect reduces the quantity of ATP normally generated via succinate dehydrogenase action (Lowenstein, 1969).
The electrons derived from succinate and NADH goes to oxygen via the ETC. Notably, subsequently, the oxygen’s reduction gives rise to water molecules. Electrons’ transfer via the ETC gives rise to H+ pumping across mitochondrion membranes, resulting in proton gradients across the membranes (Lowenstein, 1969). ATP synthase utilizes the gradients to produce ATP. Notably, CoQ10, jointly with Vitamin K2, delivers electrons to Enzyme Complex III from the other enzyme complexes. As well, the lipid peroxidation is inhibited by CoQ10 since it prevents LOO (lipid peroxyl radicals) production (Kay & Weitzman, 1987).
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