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Effects of 25-hydroxycholesterol and aminoglutethimide in isolated rat adrenal cells. A model for congenital lipoid adrenal hyperplasia?

Authors
Journal
Molecular and Cellular Endocrinology
0303-7207
Publisher
Elsevier
Publication Date
Volume
4
Issue
2
Identifiers
DOI: 10.1016/0303-7207(76)90030-7
Keywords
  • Adrenal Cells
  • 25-Hydroxycholesterol
  • Acth
  • Aminoglutethimide
  • Congenital Lipoid Adrenal Hyperplasia

Abstract

Abstract The production of corticosterone from 25-hydroxycholesterol by isolated rat adrenal cells is inhibited by aminoglutethimide phosphate (AGI); half-maximal inhibition is obtained at ca. 10 μM. AGI also inhibits ACTH-stimulated steroid production from endogeneous substrates; here half-maximal inhibition is obtained with ca. 40 μM AGI. In the presence of ACTH + AGI, 25-hydroxycholesterol causes additive inhibition. This effect of 25-hydroxycholesterol is dose-dependent. ACTH-stimulated steroid production from endogeneous substrates is partially inhibited by 5-cholene-3β, 24-diol. These results may just reflect substrate competition for the side-chain cleaving system or may be due to some secondary toxic effect on the cells.

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