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 Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mason, J. I. Articles by Korte, K. Search for Related Content PubMed PubMed Citation Articles by Mason, J. I. Articles by Korte, K.

Steroidogenesis in Dispersed Cells of Human Fetal Adrenal^*

The Cecil H. and Ida Green Center for Reproductive Biology Sciences and the Departments of Biochemistry and Obstetrics-Gynecology, The University of Texas Health Science Center, Dallas, Texas 75235

Address all correspondence and requests for reprints to: Dr. J. Ian Mason, Cecil H. and Ida Green Center for Reproductive Biology Sciences, The University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

Steroidogenesis in dispersed fetal zone cells of midtrimester human fetal adrenal was stimulated acutely by ACTH. Polypeptide hormones such as hCG, MSH, ovine PRL, and LH did not produce a similar stimulation of steroidogenesis. The principal steroid products of ACTH-stimulated fetal adrenal cells were dehydroisoandrosterone sulfate, pregnenolone, pregnenolone sulfate, and 17-hydroxypregnenolone. Only minimal production of the ⁴-3-ketosteroids, cortisol, corticosterone, and progesterone, was observed. Cyanoketone (2-cyano-4,4,17-trimethyl-17β-hydroxyandrost-5-en-3-one; an inhibitor of 3β-hydroxysteroid dehydrogenase activity) treatment of the cells caused only a minor increase in 3β-hydroxysteroid formation, confirming that 3β-hydroxysteroid formation is the principal steroidogenic fate of cholesterol in these cells. SU-10603 [7-chloro-3,4-dihydro-2-(3-pyridyl)naphthalen-1-(2H)one; a steroid 17-hydroxylase inhibitor] treatment of the cells caused a marked accumulation of pregnenolone sulfate, indicating that the C-19 steroids are produced from C-21 steroids in this tissue and possibly that dehydroisoandrosterone sulfate is synthesized directly from pregnenolone sulfate. ACTH-stimulated pregnenolone synthesis was inhibited by AY-9944 [trans-1,4-bis-(2-chlorobenzylaminomethyl) cyclohexane dihydrochloride; an inhibitor of cholesterol biosynthesis]. Thus, cholesterol synthesized de novo was the likely steroidogenic precursor in the acute hormonally stimulated fetal adrenal cells. (J Clin Endocrinol Metab 56: 1057, 1983)

^* This work was supported in part by NIH Grant 5-P50-HD-11149 and DFG Grant 1–3, Ko 772/1–2 (Federal Republic of Germany).

Received September 24, 1982.

This article has been cited by other articles:

				K. Saner-Amigh, B. A. Mayhew, F. Mantero, F. Schiavi, P. C. White, C. V. Rao, and W. E. Rainey Elevated Expression of Luteinizing Hormone Receptor in Aldosterone-Producing Adenomas J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 1136 - 1142. [Abstract] [Full Text] [PDF]