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Cyproterone acetate, a synthetic steroid hormone, is a hydroxyprogesterone derivative. The structural formula is shown in Figure I. HJC CI CH.

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The effect of cyproterone acetate (CA) on experimentally induced benign prostatic hyperplasia (BPH) in the castrated dog was investigated. BPH was induced by 6 months' treatment with 3\g=a\-androstanediol (3\g=a\-diol) alone and in combination with 17\g=b\-oestradiol(Oe2). RNA, DNA and zinc content of the glands were determined in addition to histological examination and measurement of the prostates. Two different types of prostatic enlargement were observed. First, 3\g=a\-diolinduced typical diffuse canine hyperplasia with replacement of functional activity. DNA, RNA and the zinc content of total glands were increased compared with intact controls.

Treatment of adult male rats with oestradiol, cyproterone acetate or cyproterone affected spermatogenesis, accessory sexual glands and fertility in different ways. Suppression of Leydig cells, spermatogenesis, accessory sexual glands and fertility ran parallel in oestradiol-treated animals. High doses of cyproterone acetate caused severe suppression of the accessory sexual glands and fertility but had only a slight inhibitory influence on spermatogenesis, Leydig cells were only temporarily affected. With high doses of cyproterone, Leydig cells were over-stimulated initially but returned to normal appearance during treatment. There was almost no effect on spermatogenesis but the accessory sexual gland weights and fertility were markedly reduced. Recovery from any changes was rapid after cessation of cyproterone acetate and cyproterone treatment but not after oestradiol. Lower doses of cyproterone acetate and cyproterone did not affect testicular morphology but significantly depressed the accessory sexual gland weights. Different mechanisms of action for the three steroids are discussed. Objections are raised against the use of cyproterone acetate for the control of male fertility.

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The capacity of various androgens to virilize the differentiating mammary gland in the female rat fetus has been determined. Testosterone, 5alpha-androstane-3alpha, 17beta-diol (3alpha-diol), and dihydrotestosterone (DHT) virilize the anlagen of the mammary gland by suppressing nipple formation but 5alpha-androstane-3beta, 17beta-diol, androsterone, and dehydroepiandrosterone sulfate do not affect female mammary differentiation. However, unlike the genitalia and wolffian ducts of the female rat fetus in which the masculinizing potency of DHT and 3alpha-diol is greater than that of testosterone, testosterone is more potent than its metabolites DHT and 3alpha-diol, in virilizing the mammary gland. The results suggest that testosterone is the fetal androgen mediating masculine development of the mammary gland.