This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via Google Scholar Google Scholar Articles by FARESE, R. V. Articles by LARSON, R. E. Search for Related Content PubMed PubMed Citation Articles by FARESE, R. V. Articles by LARSON, R. E.

Kinetic Aspects of Cycloheximide-Induced Reversal of Adrenocorticotropin Effects on Steroidogenesis and Phospholipid Metabolism in Rat Adrenal Sections in Vitro^*

Veterans Administration Hospital and the Department of Medicine, University of South Florida College of Medicine, Tampa, Florida 33612

Address requests for reprints to: Dr. Robert V. Farese, James A. Haley Veterans Hospital, 13000 North 30th Street, Tampa, Florida 33612.

Abstract

We examined the rate of cycloheximide-induced reversal of ACTH effects on steroidogenesis and phospholipid metabolism in adrenal sections in vitro. In the absence of cycloheximide, ACTH treatment elicited sustained increases in steroidogenesis (3- to 5-fold) and adrenal concentrations (2-fold) of phosphatidic acid, phosphatidylinositol, and polyphosphoinositides. These increases in phospholipids were not dependent on steroidogenesis, since they were also apparent in aminoglutethimide- blocked adrenal sections. The addition of cycloheximide 30 min after ACTH treatment reversed the stimulatory effects of ACTH on steroidogenesis and phospholipids, and the rates of decay for both processes were identical, viz 28 min. This relatively slow turnover in adrenal sections in vitro contrasts with a much more rapid turnover observed previously in vivo and presently in dispersed adrenal cells in vitro; thus, it appears that an artefact of the in vitro adrenal section system stabilizes the putative labile protein. More importantly, the identical rates of decay for steroidogenesis and phospholipids suggest that the same labile protein is required for both phospholipid metabolism and steroidogenesis. These findings are in keeping with our postulate that the labile protein is required for phospholipid metabolism, which, in turn, is required for steroidogenesis.

Footnotes

^* This work was supported by funds from the Research Service of the V.A.

Received March 5, 1981.