In VitroAdrenal Mitochondrial 11/3-Hydroxylation Followingin VivoAdrenal Stimulation or Inhibition: Enhanced Substrate Utilization

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Abstract
Adrenal mitochondria from rats administered 7 daily injections of either ACTH or the synthetic steroid, cyanotrimethylandrostenolone (CTA), showed increased utilization of isocitrate, succinate or malate for support of in vitro 11β3-hydroxylation of deoxycorticosterone into corticosterone (B). Short-term treatment, 1, 2 or 24 hr, resulted in increased utilization of succinate or malate but led to decreased utilization of isocitrate by the experimental groups. A study of the activities of mitochondrial isocitric dehydrogenase, malic enzyme and malic dehydrogenase was undertaken in adrenal tissue obtained after short- and long-term treatment with CTA and ACTH. The activity of malic enzyme was markedly lower than that of malic dehydrogenase. The evidence does suggest that the enzyme activities are increased following ACTH or CTA. It is likely that the response to CTA reflects in vivo release of ACTH. The increased substrate-supported B production in vitro is probably related to an effect of ACTH on mitochondrial enzymes including cytochrome-P45o.

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