Neonatal exposure of male rats to estradiol benzoate causes rete testis dilation and backflow impairment of spermatogenesis.

Estrogens administered to perinatal rodents cause spermatogenesis impairment; this study was undertaken to determine the mechanisms by which estrogens exert this effect. Neonatal male Wistar rats received estradiol benzoate (either 0.5 mg/5g BW or 1 mg/5g BW) and were killed at days 10, 22, 33, 45, and 60. Controls received vehicle. In tubule cross-sections of transverse sections of the right testes, 1) tubular diameter (TD) and seminiferous epithelium height (SEH) were measured, 2) normal and impaired spermatogenesis were classified in terms of the most advanced germ cell type present, including tubules lined by Sertoli cells only. A significant dose-dependent rise in the tubule percentage lined by Sertoli cells only at day 60 reflected spermatogenesis impairment. This was evidenced by the presence of multinucleated germ cells in a thin epithelium and sloughed into an enlarged tubular lumen, which was reflected in a significant dose-dependent increase in TD/SEH values from day 22 onward. TD was significantly greater and SEH significantly lower in tubular segments located at the cranial than the caudal halves of rat testes treated with the high (days 22, 33, and 60) and the low dose (day 33). This indicated distension in cranial tubular segments, perhaps due to the fact that these segments were the closest to the dilated rete testis. Consequently, they showed the highest TD/SEH values and the most regressive features of spermatogenesis (tubules lined by Sertoli cells only). In contrast, caudal segments in rat testes treated with the low dose showing TD/SEH values similar to controls displayed a delayed maturation of spermatogenesis coinciding with the late appearance of mature Leydig cells.