TCA Cycle

overview of TCA Cycle

-entry of carbon atoms into cycle is through acetyl CoA (from carbohydrates, fatty acids, amino acids, and ethanol) 

-accounts for most of ATP generated through fuel oxidation by producing reduced cofactors NADH and FADH2

-in presence of O2, reduced cofactors can be oxidized by electron transport chain to yield ATP 

energy yield of TCA Cycle

-2.5 ATP per NADH and 1.5 ATP per FADH2

-TCA Cycle generates 3 NADH, 1 FADH2, and 1 GTP

-oxidation of one molecule of acetyl-CoA gives 10 molecules of ATP under aerobic conditions

pyruvate dehydrogenase that converts pyruvate to acetyl CoA is activated and inhibited by what

activated by insulin and inhibited by NADH

critical regulators of TCA Cycle

-oxaloacetate, acetyl CoA, citrate, and NADH

-substrate availability and product inhibition regulate citrate synthesis

-NADH regulates cycle through product inhibition

connection of TCA cycle to other pathways

-provides malate (oxidized to oxaloacetate) for gluconeogenesis

-provides citrate for cytosolic fatty acid synthesis

-amino acid biosynthesis uses TCA cycle intermediates

-explains why TCA Cycle is both catabolic and anabolic

key molecules and drugs to know for TCA Cycle

• Acetyl-CoA: Entry molecule for TCA; combines with oxaloacetate to form citrate.

• NAD⁺ / NADH: Electron carrier; NAD⁺ accepts electrons, NADH stores energy for ATP production.

• FAD / FADH₂: Electron carrier; FAD accepts electrons, FADH₂ donates to ETC for ATP generation.

• Pyruvate: End product of glycolysis; converted to acetyl-CoA before entering TCA.

• Citrate: First TCA intermediate; formed from acetyl-CoA + oxaloacetate.

• Oxaloacetate: TCA cycle acceptor molecule; regenerates at end of cycle to combine with acetyl-CoA.

• Pyruvate dehydrogenase complex (PDC): Converts pyruvate → acetyl-CoA, linking glycolysis to TCA.