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Effect of male sex hormones on ascorbic acid metabolism in rats.

Castrated male rats were injected intramuscularly with testosterone (5mg/day) and dehydroepiandrosterone (5mg/day) continuously for two weeks. Animals were sacrificed and the various metabolites of ascorbic acid in liver and urine were determined. Total ascorbic acid and the activities of hepatic ascorbic acid synthesizing enzymes were also determined. The activities of both liver and kidney ascorbic acid degrading enzymes were studied. In contrast to testosterone, dehydroepiandrosterone failed to modify the ascorbic acid metabolism in castrated rats. Testosterone administration to castrated rats was found to restore the hepatic contents of as-corbic acid metabolites to the sham control levels. It was suggested that the functional OH group at C-17 in androgens might have some role in as-corbic acid metabolism. Castration was found to cause decrease in the activities of two out of the three biosynthetic enzymes of ascorbic acid, namely D-glucurono-δ-lactone hydrolase and L-gulono-γ-lactone oxidase in rat liver. The activity of L-gulono-γ-lactone hydrolase was found to be unchanged in castration. This result which is in slight disagreement with the earlier work of STUBBS et al. has been discussed. Testosterone was observed to restore the decrease in the activities of both D-glucurono-δ-lactone hydrolase and L-gulono-γ-lactone oxidase in castrated rats. Testosterone was also found to restore the increased activity of both renal and hepatic dehydroascorbatase observed in castration to the level of sham control rats. However, exogeneous administration of testosterone intramuscularly (5mg/day) for two weeks to normal rats did not show any significant alteration in the ascorbic acid metabolism.