Pyruvate metabolism in rat brain mitochondria.
1. Oxidation of pyruvate by rat brain mitochondria was stimulated in state 3 by malate or succinate up to 250 nmoles O2/mg protein/min. Oxidation of malate, succinate, 2-oxoglutarate or glutamate as the sole substrates, was 1/4 - 1/5 that observed with pyruvate. 2. Maximum oxygen consumption in state 3 was observed at pH 6.90 - 7.20, whereas in state 4 it was not affected by changes in pH. 3. In state 4, in the absence of exogenous acceptor or acetyl residues, acetate was the main oxidation product, corresponding to about 80% of the amount of pyruvate utilized. Malate did not affect the rate of pyruvate utilization but lowered acetate concentration and raised concentration of citrate and 2-oxoglutarate. 4. In state 3, pyruvate and malate were converted mainly to 2-oxoglutarate, its concentration being three times as high as that of citrate. 5. Formation of citrate, 2-oxoglutarate and acetate from pyruvate in brain is considered as a function of availability of the acceptor of acetyl residues and the energy state of mitochondrion.
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000648:ultrastructure; D006863:Hydrogen-Ion Concentration; D008274:Magnesium / Q000494:pharmacology; D008928:Mitochondria / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D011773:Pyruvates / Q000378:metabolism*; D051381:Rats
D011773:Pyruvates; D000255:Adenosine Triphosphate; D008274:Magnesium