Glutamate metabolism in rat kidney mitochondria.
1. Kidney cortex mitochondria did not swell in ammonium or potassium salts of glutamate even in the presence of valinomycin or 2,4-dinitrophenol. Aminooxyacetate diminished the reduction of nicotinamide nucleotides in intact mitochondria in the presence of glutamate. 2. Transamination with oxaloacetate appeared to be the main pathway of glutamate metabolism in isolated rat kidney cortex mitochondria under various metabolic conditions. Ammonia formation was negligible. The gamma-aminobutyrate pathway was found to be of almost no importance.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000625:Aminooxyacetic Acid / Q000494:pharmacology; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D004140:Dinitrophenols / Q000494:pharmacology; D005971:Glutamates / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D008933:Mitochondrial Swelling / Q000187:drug effects; D010071:Oxaloacetates / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D014634:Valinomycin / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D004140:Dinitrophenols; D005971:Glutamates; D010071:Oxaloacetates; D000625:Aminooxyacetic Acid; D014634:Valinomycin; D005680:gamma-Aminobutyric Acid; D000244:Adenosine Diphosphate; D000641:Ammonia