Relation of the pituitary gland to gonadal hormone effects on the adrenocortical 11beta-hydroxylase system in rats.
Steroids, 1975/6;25(6):707-16.
Kramer RE, Greiner JW, Colby HD
PMID: 168671
Impact factor: 2.76
Abstract
Studies were conducted to further examine the mechanisms responsible for gonadal hormone effects on the rat adrenocortical 11beta-hydroxylase system. Despite higher concentrations of cytochrome P-450 and larger 11-deoxycorticosterone (DOC)-induced difference spectra in adrenal mitochondria from females than males, no sex difference in 11beta-hydroxylase activity was observed. The pregnenolone-induced difference spectrum, indicative of cholesterol binding to cytochrome P-450, also was similar in males and females. Testosterone administration to castrated males lowered both 11beta-hydroxylase activity and mitochondrial cytochrome P-450 content. Estradiol produced the opposite effects in castrated females. However, when given to ACTH-replaced hypophysectomized rats, neither testosterone nor estradiol affected cytochrome P-450 levels or the rate of 11beta-hydroxylation. These observations, taken with the known effects of estradiol and testosterone on ACTH secretion in rats and the effects of ACTH on 11beta-hydroxylation, indicate that gonadal hormone effects on the 11beta-hydroxylase system are mediated by ACTH.
MeSH terms
Adrenal Glands; Adrenocorticotropic Hormone; Animals; Castration; Corticosterone; Cytochrome P-450 Enzyme System; Estradiol; Female; Hypophysectomy; Male; Mitochondria; Organ Size; Ovary; Pregnenolone; Rats; Spectrophotometry; Steroid Hydroxylases; Testis; Testosterone
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