Demonstration of direct effect of estrogen on rat spermatogenesis.

The presence of an estrogen receptor in Leydig cell cytosol suggests that estrogen could have a direct action on Leydig cell function. We have shown earlier the direct effect of estradiol on testosterone biosynthesis. We report in this communication effect of estradiol on spermatogenesis using hypophysectomized rats treated daily for four days with 400 IU hCG/Pregnyl) and 1 IU FSH (Pergonal), a model that eliminates the possibility of feedback effects of estradiol on gonadotropin secretion. Estradiol was administered in subcutaneous silastic capsules. The control animals had empty capsules. The inhibition of spermatogenesis, after estradiol treatment, was marked by the presence of multinucleated giant cells, disorganization of the germinal elements, accumulation of cellular debris and the absence of late spermatid and spermatozoa. These changes in the histoarchitecture of testis were accompanied by the reduction in the diameter of the seminiferous tubules and the thickness of the basement membrane. Morphologically Leydig cells were, however, normal. Inhibition of spermatogenesis was in relation to the amount of estrogen available/administered as estradiol capsule of 0.25 cm did not evoke significant changes in the histology of the testis whereas estradiol capsule of 4 cm caused maximum damage to the spermatogenesis. Similarly progressive damage to the spermatogenesis was quite apparent as the number of days increased after estradiol capsule implantation. Neither high (1600 IU/day/4 days) nor low /5.25 IU/day) doses of hCG synergized the effect of estradiol on spermatogenesis. Testis weight was significantly reduced after estradiol treatment but weight of the epididymis and accessory sex organs did not change. Body weight was also not effected by estradiol treatment.