The Krebs Cycle, also known as the Citric Acid Cycle or Tricarboxylic Acid Cycle, is a key metabolic pathway occurring in the mitochondrial matrix.
It plays a critical role in cellular respiration, allowing for ATP production by providing reduced electron carriers for the Electron Transport System (ETS).
Relationship with Electron Transport System
ETS requires NADH and FADH2 to function; these are supplied by the Krebs Cycle.
Oxygen is required for ETS and indirectly for the Krebs Cycle to function effectively.
Krebs Cycle Steps
Formation of Citrate:
Acetyl CoA combines with oxaloacetate to form citrate.
Initiated by an enzyme that binds both molecules, facilitating their reaction.
Isomerization to Isocitrate:
Citrate is converted to isocitrate by removing and reattaching water in a different configuration.
Enzyme involved is aconitase.
Oxidation and Decarboxylation:
Isocitrate is oxidized to alpha-ketoglutarate, producing NADH and releasing CO2.
A secondary alcohol group is oxidized to a ketone.
Further Oxidation:
Alpha-ketoglutarate is converted to succinyl-CoA, releasing another CO2 and producing NADH.
Succinyl-CoA is transformed into succinate, generating GTP, which can be converted to ATP.
Formation of Fumarate:
Succinate is oxidized to fumarate, producing FADH2.
This step involves the creation of a carbon-carbon double bond.
Hydration to Malate:
Fumarate is hydrated to malate by adding water.
Final Oxidation:
Malate is oxidized to regenerate oxaloacetate, producing NADH.
Key Points
The cycle produces 3 NADH, 1 FADH2, 1 GTP (converted to ATP), and releases 2 CO2 per acetyl CoA.
No ATP is directly produced in the Krebs Cycle; ATP is generated in the ETS using NADH and FADH2.
Additional Insights
The cycle is crucial for energy production under aerobic conditions.
If components of the ETS are inhibited, this can impact ATP yield.
Complex metabolic control mechanisms ensure balance between cycle substrates and products.