Antifertility effects of estradiol in adult male rats

The dose-related effects of estradiol 17-beta at the doses 0.1 mug, 10 mug, 100 mug, 200 mug, 300 mug, 400 mug, 1000 mug/kg/day were determined on sperm motility, potency, fertility parameters, serum levels of LH, FSH, PRL and testosterone, weights of testes and accessory sex organs, weights of pituitary and adrenal glands. The drug was administered daily via sc route for a period of 60 days. Dose-related effects on fertility parameters of the estradiol-treated male rats were ascertained by allowing them to mate With normal cycling female rats. Estradiol at 0.1 mug/kg/day dose significantly reduced sperm motility with no effects seen on potency or fecundity, serum LH, FSH, PRL or testosterone, weights of testes and accessory sex organs while pituitary weight increased. Estradiol at 10 mug/kg/day dose significantly reduced motility, serum LH, FSH, weights of testes and accessory sex organs, while pituitary weight increased with no effects seen on potency, fecundity, PRL or testosterone. Estradiol at 100-1000 mug/kg/day dose significantly reduced motility, potency and fecundity, serum LH, FSH and testosterone, weights of testes and accessory sex organs while serum PRL and the weights of pituitary and adrenal glands increased significantly. Histology of the testes revealed disorganization of the cytoarchitecture in the seminiferous tubules, vacuolation, absence of lumen and compartmentalization of spermatogenesis. Estradiol withdrawal, testosterone propionate at 100 mug/kg/day or antiestrogen (tamoxifen citrate) at 400 mug/kg/day prevented the histological changes. It is concluded that estradiol reduces sperm motility even at a low dose. Low doses (<10 <mu>g/kg/ day) appear to maintain whilst high doses (>10 mug/kg/day) reversibly disrupt spermatogenesis. Prevention of disruption by testosterone or antiestrogen indicates crosstalk between androgen and estrogen receptors in Sertoli cells. Loss of potency and fecundity also suggests effects on crosstalk between these receptors in other male reproductive organs. (J. Endocrinol. Invest. 24: 598-607, 2001) (C) 2001, Editrice Kurtis.