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In comparison to testosterone, 18 beta-hydroxy-18 alpha-methyl-16 alpha-methylene-D-homo-5 alpha-androstane-3-one (D-homo-S) shows more pronounced anti-gonadotrophic than androgenic properties in rats. The present study was initiated in rabbits to investigate the potential of D-homo-S to suppress spermatogenesis. D-homo-S in sesame oil was administered at the doses of 0.1 (DI), 3 (D II) or 10 mg (D III) per rabbit each day for 8 weeks. During treatment serum testosterone, sperm concentration and quality of sperm motility decreased, whereas sex drive, semen volume and seminal plasma concentrations of fructose and zinc were not changed in any of the groups. Testicular weight and intratesticular testosterone concentration decreased significantly in groups D II and D III, while weights of accessory sex glands increased in those groups. Testosterone in the same dose regimen did not suppress sperm count, motility or serum testosterone, however, seminal plasma zinc concentration in group T III and fructose in group TI increased. Testicular weight and intratesticular testosterone concentration decreased in group TIII only. On the other hand, the weight of the accessory sex glands increased in the same group. In conclusion, D-homo-S suppresses spermatogenesis and increases accessory sex gland weights at doses, when testosterone is still ineffective. Thus, in rabbits D-homo-S appears to be a more potent androgen than testosterone but a dissociation between antigonadotrophic and androgenic properties could not be observed.

16 female rabbits were actively immunized against testosterone (T). 9 of them conceived and gave birth to 89 neonates. In all neonatal plasma samples antibodies against T were detected. In the males the plasma T levels were elevated 1,000-fold. The testes of these animals were examined by means of morphometrical and biochemical methods. The results indicate increased stimulation of Leydig cells in fetuses exposed to antibodies against T, and suggest that even in the fetus a negative feedback is acting between testes and hypothalamo-pituitary system, which is interrupted by the antibodies which bind and inactivate T.

Subcutaneous treatment of immature male rats with an estrogen precursor, 19-hydroxy-testosterone (19-OHT), at a daily dose of 1 mg/animal for 14 days leads to a significant decrease in the weight of testis, ventral prostate and seminal vesicle. The peripheral levels of LH are lowered. Testicular histology indicates that the effects of 19-OHT are very similar to the known of effect induced by estradiol-17 beta. 19OHT induces a marked impairment of spermato- and spermiogenesis. The maturation division is completely inhibited. The effect of 19-OHT on spermatogenesis is partially reversed by concomitant administration of an aromatase inhibitor (4-acetoxy-4-androstene-3.17-dione, (4-AA] at a dose of 1 mg/animal/day s.c. Meiotic activity is restored, and the weights of genital organs and the serum LH values increase. 4-AA alone has no appreciable effect on the parameters examined in this study. The present results suggest that specific inhibitors of estrogen biosynthesis might not only be useful to investigate the patho-physiological role of estrogens on spermatogenesis, but also be suitable to some extent for the treatment of estrogen-induced infertility in men suffering from idiopathic oligozoospermia.

The treatment of adult male Wistar rats with a LHRH-agonist (lutrelin Wyeth/WY 40972) resulted in severe damage of the seminiferous tubules as well as in remarkable changes of the blood vessels within 24 hours. First striking signs of alterations within the blood vessels were already found 6 hours after the injection of lutrelin: the blood vessels were almost totally filled with leucocytes. Neither the effects on the germinal epithelium nor the effects on the blood vessels were prevented by the simultaneous treatment with 3 mg testosterone propionate (TP). The treatment with indomethacin, however, clearly antagonized both events. The complete inefficiency of TP to overcome the inhibitory effects of lutrelin on the testes does argue against an androgen deficiency as the primary cause. The results obtained with indomethacin strengthen the hypothesis, that the early deleterious effects of LHRH-agonists on the germinal epithelium of the rat are primarily caused by circulatory disturbances in the testes and that prostaglandins may act as mediators.

Twelve patients with prostatic carcinoma in stage C or D underwent subcapsular orchiectomy. Testosterone serum concentrations were measured by radioimmunoassay before and up to eight months following orchiectomy. After an initial decrease, testosterone concentrations remained between 0.42 ng and 0.67 ng/ml serum throughout the observation period. Stimulation with 5000 IU hCG/day for three days did not cause an increase in testosterone concentrations.

The in vitro release and biological effectiveness of silicone rubber implants containing testosterone in orchidectomized male rats was investigated over a period of 20 weeks. A marked reduction in release in 0.9% saline solution could be observed in vitro relative to the incubation time in the medium. The reduction in release was greatest during the first few weeks of the experiment. Rat seminal vesicles and prostates, which were greatly stimulated at the start of the experiment, lost weight corresponding to the release rate in vitro. The implants containing testosterone used here were 4 to 26 times more effective than testosterone propionate injected s.c.