Rat adrenal tissue in vitro oxidized 17o;-methylandrost-5-ene-3j3, 17/3-diol (MAD) to 17a-methylandrost-4-en-17j3-ol-3-one (17«-methyltestosterone). Both MAD and 17o-methyltestosterone were further metabolized to at least 5 ultraviolet light-absorbing products. Evidence was obtained for the identification of the major product as ll/3-hydroxy-17a-methyltestosterone. The next most abundant product was probably ll-oxo-17a-methyltestosterone. The other products were formed in lesser amounts and little progress was made in their identification. The metabolism of 17a-methyltestosterone to these metabolites was strongly inhibited by the addition of Metopirone to the incubation medium, suggesting that hydroxylation is a major pathway of metabolism. {Endocrinology 81: 1278, 1967) I N 1959, Saffran and Vogt (1) observed that the administration of MAD 6 to rats decreased the secretion of corticosterone in adrenal venous blood. The experiments described in this paper present evidence for the oxidation of MAD to 17a-methyltestosterone and for the further metabolism of 17a-methyltestosterone by the rat adrenal 6 Abbreviations and trivial names used in this paper: MAD = 17a-methylandrostenediol = 17a-methylandrost-5-ene-3/3, 17/3-diol; 17a-methyltestosterone = 17a-methylandrost-4-en-17/3-ol-3-one. gland in vitro. The effects of MAD and 17a-methyltestosterone on the formation of steroids by the rat adrenal in vitro will be described elsewhere.
Materials and MethodsAdrenals. In most experiments, young adult male rats derived from the Sprague-Dawley strain (Canadian Breeding Laboratories, St. Constant, Que.), weighing in the range of 150 to 250 g, were used. Rats of relatively uniform body weight ( ± 10 g) were used in each experiment. The rats were anesthetized with an intraperitoneal injection of 4 mg/100 g body weight of sodium pentobarbital and were decapitated. The adrenal glands were removed, freed of adhering fat and carefully quartered with fine scissors.
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