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Trilostane is a competitive inhibitor of 3beta-hydroxysteroid dehydrogenase. In vitro, the drug inhibits conversion of pregnenolone to progesterone but does not alter conversion of cholesterol to pregnenolone nor progesterone to corticoid hormones. When given orally to rats, trilostane inhibits corticosterone and aldosterone production and elevates(More)
Trilostane inhibits adrenal, ovarian, and placental steroidogenesis when administered orally to rhesus monkeys. By inhibiting 3 beta-hydroxysteroid dehydrogenase activity, it causes an increase in circulating levels of pregnenolone. Trilostane reverses the stimulation of luteal progesterone production and the delay in onset on menstruation induced by human(More)
1. Aerobic incubation of [(14)C]oestradiol, in the presence of surviving gut tissue of the sea urchin Strongylocentrotus franciscanus, or a soluble enzyme system prepared therefrom, resulted in rapid formation of a water-soluble metabolite, identified as oestradiol 3-sulphate. 2. No evidence was obtained for the formation of other metabolic derivatives by(More)
In rats treated with furosemide, urinary losses of water, sodium and potassium were accompanied by increased circulating levels of aldosterone. Trilostane, an inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase activity, prevented furosemide-induced hyperaldosteronism which resulted in a partial inhibition of diuretic-induced kaliuresis without a(More)
Azastene is an orally effective "luteolytic" agent in rhesus monkeys. In nonpregnant monkeys it reverses the human chorionic gonadotropin-stimulated increase in progesterone production and delay in the onset of menstruation, and, in inseminated monkeys, it prevents pregnancy if given for 5 days beginning on day 24 of the menstrual cycle. The drug is also(More)
Topterone, 17 alpha-propyltestosterone, was administered parenterally or topically to rats, rabbits or hamsters to determine its endocrine profile. Systemic administration demonstrated that topterone was both antiandrogenic and progestational. Topical application failed to elicit a systemic antiandrogenic response at 1 g/kg/day and only a minimal(More)
Adenosine 3'5'-cyclic phosphate stimulated the conversion of added cholesterol to pregnenolone in "coupled" rat adrenal mitochondria provided with succinate, and in "leaky" mitochondria fortified with reduced nicotinamide adenine dinucleotide phosphate. Adenine nucleotides other than adenosine 3',5'-cyclic phosphate did not duplicate these actions. The(More)