Chance 1962 J Biol Chem
|Chance B, Hagihara B (1962) Activation and inhibition of succinate oxidation following adenosine diphosphate supplements to pigeon heart mitochondria. J Biol Chem 237:3540-5.|
Abstract: 1. In succinate oxidation reactivated by a low concentration of adenosine triphosphate, addition of small amounts of adenosine diphosphatc will lead to reestablishment of the inhibited state of succinate oxidation after a short burst of respiration.
2. The inhibited state is not relieved by either phosphate or phosphate acceptors.
3. The inhibition is closely correlated with a high degree of oxidation of mitochondrial reduced diphosphopyridine nucleotide, which occurs immediately on addition of adenosine diphosphate and is followed by the inhibition of succinate oxidation after the oxidation or rather small amounts of succinate.
4. Oxidation of more than approximately two-thirds of the total diphosphopyridinc nuclcotide (DPN) reducible by succinate and adenosine triphosphate eventually leads to inhibition of succinate oxidation.
5. Based on independent evidence for a compartmentation of mitochondrial pyridine nucleotide (approximately one-third available to DPN-linked substrates), it is proposed that inhibi- tion occurs when oxidation of DPN in the compartment available to malate causes oxaloacetate formation sufficient to inhibit succinate oxidation.
6. The general possibility of DPN control of malate oxidation is considered with respect to the whole question of oxaloacetate regulation of the citric acid cycle.
• Keywords: Oxaloacetate • Bioblast editor: Gnaiger E
Labels: MiParea: Respiration
Organism: Birds Tissue;cell: Heart Preparation: Isolated mitochondria Enzyme: Complex II;succinate dehydrogenase Regulation: Flux control, Inhibitor, Redox state Coupling state: LEAK, OXPHOS, ET Pathway: S, NS