To assess the capacity of different androgens to virilize the urogenital tracts of female rat embryos, pregant rats were given varying amounts of ten steroids from day 14 of gestation until day 21. The newborn from these mothers were given 1/25 of the maternal dosage on days 1 and 3 after birth and killed on day 4. The urogenital tracts of the female embryos were assessed for the presence of the epididymis, vas deferens, seminal vesicle, and prostate. Dihydrotestosterone administration invariably produced bilateral virilization of the female urogenital tract when the maternal dosage was 8 mg/day, whereas methyltestosterone, methyldihydrotestosterone, and 3α, 17β-androstanediol produced equally marked masculinization at a 4 mg/day dosage. No virilization was noted following treatment with 5β-dihydrotestosterone, androstenedione, 3β, 17β-androstanedione, or androsterone. Testosterone in these dosages caused fetal resorption. These findings, considered together with recent studies of androgen metabolism and binding in fetal tissues, have been interpreted as support for the concept that dihydrotestosterone is the active androgen that induces male differentiation of the urogenital sinus. Furthermore, although testosterone itself probably induces virilization of the wolfnan ducts under normal physiological conditions, the finding that 5βreduced androgens share this capacity indicates that the critical receptor mechanisms in the wolffian duct are not specific for Δ4-3-ketosteroids.
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