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Short-Term Effects of Dehydroepiandrosterone Treatment in Rats on Mitochondrial Respiration¹

The Hormel Institute, University of Minnesota, Austin, MN 55912

Administration of dehydroepiandrosterone (DHEA) to rats results in alterations in liver and serum factors. This study was undertaken to determine the earliest metabolic change(s) associated with DHEA treatment. Serum cholesterol, triacylglycerol, glucose, insulin, glucagon, thyroid hormones and hepatic glucose-6-phosphate dehydrogenase activity were, in general, unaltered in obese Zucker rats after 7 d and 24, 12 and 3 h of DHEA treatment. Malic enzyme, long-chain fatty acyl-coenzyme A hydrolase and catalase activities and peroxisomal ß-oxidation rates were elevated after 7 d and 24 h of DHEA treatment, but not after 12 h. Mitochondrial ß-oxidation was not altered. Hepatic mitochondrial state 3 respiration per g liver with glutamate-malate was elevated after 7 d and 24, 12 and 3 h in DHEA-treated rats and was elevated per mg protein except after 7 d. Succinate-supported state 3 respiration per g liver was also elevated after 7 d and 24 and 12 h of DHEA treatment. Mitochondria from rats treated for 7 d had lower levels of cardiolipin and phosphatidylethanolamine and an increase in phosphatidylcholine. Changes in fatty acid composition of these phospholipids occurred after 7 d and 24 h of DHEA treatment. In an additional study, rats were treated with DHEA or DHEA plus ethidium bromide for 3 d. Ethidium bromide inhibited the increase in mitochondrial protein and respiration associated with DHEA treatment. These findings indicate that mitochondrial respiration is the earliest factor affected by DHEA and may be associated with protein synthesis.

KEY WORDS: • rats • state 3 and 4 respirations • fatty acids • phospholipids • ethidium bromide

¹ This work was supported by Program Project Grant HL08214 from the U.S. Public Health Service and by the Hormel Foundation.

² Current address: Division of Adolescent Medicine, Schneider Children's Hospital of the Long Island Jewish Medical Center, New Hyde Park, NY 11042.

³ To whom correspondence should be addressed.

Manuscript received 30 July 1990. Revision accepted 8 October 1990.