Induction of precocious maturation of spermatogenesis in infant rats by human menopausal gonadotropin and inhibition by simultaneous administration of gonadotropins and testosterone.

This study was undertaken to determine if the initiation of spermatogenesis could be modified by the administration of gonadotropins and sex hormones in infant rats. Five-day-old rats were injected daily between the 5th and 11th days of life with test substances and killed on day 15. Administration of testosterone propionate (TP; 2.5 mg daily), human menopausal gonadotropin (hMG; 7.5 IU daily), or coadministration of both of these substances (TP + hMG) or administration of estradiol benzoate (15 micrograms daily) caused quantitative changes in premeiotic spermatogenesis, as measured by the mean cell counts per tubule cross-section. hMG caused an increased yield of type A1 spermatogonia (SgA1) from undifferentiated type A spermatogonia (UnA) and increased the yield of type B spermatogonia from SgA1. TP was not effective in stimulating first premeiotic spermatogenesis, and in contrast to hMG, it had a negative influence on the numbers of UnA and SgA1 and on the volume of Sertoli cell nucleus. Administration of TP + hMG or estradiol benzoate resulted in a significant increase in the numbers of UnA and SgA1, but inhibited cell differentiation. TP + hMG significantly reduced the rate of premeiotic spermatogenesis. The results demonstrate that precocious numerical stabilization of premeiotic spermatogenesis can be achieved by the application of hMG. TP applied alone was able to induce peripheral androgenic effects (seminal vesicle weight) 100% greater than those produced by administration of hMG, but was not able to stimulate seminal tubule function. TP applied together with hMG produced inhibition of spermatogenesis. This effect might be due to the inhibition of Sertoli cell function by the direct influence of testosterone. In contrast to testosterone, estradiol may play a stimulatory role in the multiplication of the reserve stem cells of the first spermatogenesis of the rat.