Mitochondrial Aspartate Aminotransferase and the Effect of Testosterone on Citrate Production in Rat Ventral Prostate

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Abstract
Mitochondrial aspartate transamination was investigated as a major source of oxalacetate for citrate synthesis in rat ventral prostate. Citrate accumulation was measured in isolated mitochondria incubated with acetyl-CoA and various combinations of amino acids. Aspartate plus .alpha.-ketoglutarate in the presence of acetyl-CoA resulted in significant citrate accumulation. Neither aspartate nor .alpha.-ketoglutarate alone resulted in any significant citrate accumulation. Aspartate and .alpha.-ketoglutarate use was comparable to glutamate and citrate production. The results indicated the presence of a mitochondrial aspartate aminotransferase [AAT]. Castration (3 days) caused a significant decrease in citrate production from aspartate plus .alpha.-ketoglutarate and a decrease in mitochondrial AAT activity in prostate although no effect on kidney activity occurred. A single injection of 1 mg testosterone propionate to castrate rats significantly increased prostate mitochondrial AAT activity within 24 h while malate dehydrogenase activity was unaltered. A double reciprocal plot indicated that testosterone might regulate the level of mitochondrial AAT in the prostate. Ventral prostate also contains a uniquely high level of endogenous aspartate. Aspartate might be the major 4-carbon source of oxalacetate for citrate synthesis. Testosterone possibly regulates prostate citrate production by its effect on the level of mitochondrial AAT activity.