AP Syllabus focus:
‘In mitochondria, pyruvate oxidation and the Krebs cycle release electrons, reduce NAD+ and FAD, and release carbon dioxide.’
Pyruvate oxidation and the Krebs cycle form the central “link” between glycolysis and later energy-harvesting steps. They extract high-energy electrons, store them in reduced coenzymes, and release carbon dioxide as carbon is fully oxidised.
Where and why these reactions happen
In eukaryotic cells, pyruvate oxidation and the Krebs cycle (citric acid cycle) occur in the mitochondrial matrix, where enzymes are positioned to rapidly transfer carbon fragments and electrons.
These stages:
Practice Questions
FAQ
It commits pyruvate to acetyl-CoA formation, linking carbohydrate breakdown to mitochondrial oxidation.
It is strongly regulated by the balance of NADH/NAD$^+$ and acetyl-CoA/CoA, coordinating carbon entry with the cell’s capacity to oxidise it.
Usually not. In early turns, the CO$_2$ released typically comes from carbons that were already part of oxaloacetate.
The acetyl carbons become part of the regenerated oxaloacetate and are released as CO$_2$ in later turns.
Several intermediates can be diverted for biosynthesis (e.g., amino acid precursors), while the cycle simultaneously breaks down acetyl-CoA for energy capture.
Cells replenish intermediates to keep the cycle running when withdrawals occur.
It produces ATP (or GTP) directly from a high-energy intermediate without using an electron transport chain.
This provides a small but immediate ATP yield even when downstream electron processing is limited.
They use anaplerotic (“filling up”) reactions that convert other metabolites into Krebs intermediates.
A common route converts pyruvate into oxaloacetate, maintaining cycle capacity when intermediates are withdrawn for biosynthesis.
