Summary
Highlights
Acetyl CoA, derived from glucose, fatty acids, or amino acids, is crucial for the Krebs cycle. It combines with oxaloacetate to form citrate, catalyzed by citrate synthase, marking the start of the cycle. Citrate then isomerizes to isocitrate with the help of aconitase and an iron-sulfur cluster.
Isocitrate dehydrogenase converts isocitrate to alpha-ketoglutarate, releasing carbon dioxide. Vitamin B3 (niacin) acts as a co-factor, leading to the formation of NADH, which enters the electron transport chain. Magnesium ions stabilize the enzyme and substrate.
Alpha-ketoglutarate dehydrogenase converts alpha-ketoglutarate to succinyl CoA, again releasing carbon dioxide and producing NADH for the electron transport chain. Various B vitamins are essential: B1 (thiamine) for decarboxylation, B2 (riboflavin) for FAD reduction to FADH2, B3 (niacin) for NAD reduction to NADH, and B5 (pantothenic acid) as a component of coenzyme A.
Succinyl CoA is transformed into succinate by succinyl CoA synthetase. Vitamin B5 is vital for coenzyme A. A phosphate group from GTP is transferred to ADP, forming ATP through the incorporation of inorganic pyrophosphate.
Succinate is oxidized to fumarate by succinate dehydrogenase. Vitamin B2 supports the synthesis of FAD, which is then reduced to FADH2. This FADH2 then proceeds to the electron transport chain.
Fumarate hydratase (fumarase) adds water to fumarate, forming malate. Malate dehydrogenase then oxidizes malate to oxaloacetate, reducing NAD to NADH in the process. Vitamin B3 is critical for NAD's structure and function. This regenerates oxaloacetate, completing the Krebs cycle and facilitating continuous energy production for cellular respiration.