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Developmental, hormonal, and gametogenic parameters were evaluated in male progeny following chronic dietary exposure to the phytoestrogen genistein. Twenty pregnant rats were fed a diet containing genistein (50 microg/d) from d 17 of gestation, and 12 were fed a control diet without genistein. Four litters each of control and genistein-fed rats were euthanized on d 21. The remaining pups were weaned on d 21 and only male rats were used in this study. On d 21, eight litters of genistein-fed rats were placed on control diet (gestational and lactational exposure alone [GL-G]), and the remaining eight continued on genistein diet (lifelong exposure group [LL-G]). These rats were euthanized (four litters/group) on d 70 or 130 of life. Serum testosterone, which was slightly reduced in genistein-exposed rats on d 21, did not differ among treatment and control groups on d 70 and 130. Serum luteinizing hormone of genistein-exposed rats was reduced on d 21 and 130, but not on d 70. Serum follicle-stimulating hormone did not vary among groups at any age. Treatment-related effects of dietary genistein were not observed on the weights of the testes of 21-d-old rats. Except for a slight decrease in testis weight of GL-G rats at 130 d, no significant effect of dietary exposure was observed on the weight of the testes in any other group. However, epididymal weights were significantly reduced in both treated groups at d 130. Testicular sperm count (on d 70 as well as 130) also was not affected in GL-G or LL-G rats. We conclude that gestational plus lactational exposure to genistein and subsequent dietary exposure to genistein have no adverse effects on gametogenic function in male rats.

The objective of this study was to determine the effects of neonatal exposure to phytoestrogens on male reproductive function as adults. Male rats were injected either with 100 micrograms coumestrol or DMSO (controls) daily during their first 5 d of life. Pituitary gland, testes, sex accessory organs, and blood were collected on d 60 of life. Serum testosterone, LH, and FSH levels were determined by RIA. Levels of steady-state mRNA for gonadotrophin subunits (LH beta and FSH beta were determined by Northern blot analysis and quantified by a scanning densitometer. Coumestrol had no effect on weights of testes and sex accessory organs, or sperm count. Similarly, there were no significant differences among serum concentrations of testosterone, LH beta and FSH of coumestrol-treated rats and those of controls. Whereas steady state levels of LH beta mRNA in coumestrol-treated rats did not differ from those of controls, steady state levels of FSH beta mRNA increased (37%) in treated animals. However, the augmented FSH beta mRNA expression in coumestrol-treated rats did not negatively affect reproductive potential in male rats. We conclude that neonatal exposure to coumestrol does not alter reproductive organ structure or spermatogenic potential in male rats.

Male hormonal contraception has been limited to date because two fundamental requirements have not been concurrently satisfied, these are, consistent and dependable azoospermia and infertility coupled with maintenance of libido. The objective of this study was to determine the extent to which implants of potent androgen (DHT) will restore androgenization and spermatogenesis in hypogonadotropic infertile male rats. Twenty-five sexually mature male rats of proven fertility were actively immunized against gonadotropin releasing hormone (GnRH) to induce azoospermia. After azoospermia was achieved, GnRH immunized rats received subdermal DHT-filled Silastic implants of 2, 4, 6, or 8 cm, or empty implants (n=5/group). Five untreated control rats received empty capsules. Eight weeks later, fertility was evaluated, sperm number was obtained from the testis, and weights of androgen-dependent organs were measured. The results indicate that immunoneutralization of GnRH induced complete azoospermia, and subsequent treatment with DHT implants of 2 or 4 cm for 8 wk restored accessory organ weights, but did not restore spermatogenesis or fertility. In addition, DHT implants of 6 to 8 cm partially restored spermatogenesis, but not fertility. We conclude that low-dose DHT supplementation of GnRH-immunized rats may be a suitable alternate therapy able to maintain androgenization in the face of persistent azoospermia in the rat. This may be an effective model for development of a male contraceptive.