Effects of short- and long-term administration of tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced steroidogenic lesion.
hCG-induced testicular desensitization is characterized by inhibition at the level of the C-17,20-lyase enzyme. This defect has been attributed to an early rise in oestradiol (E2) following hCG administration. To test this hypothesis the E2-receptor antagonist, tamoxifen, was employed. From in vitro studies the evidence suggests that tamoxifen depletes the E2-receptor within 24 h. In this in vivo study, short-term (36 h) administration of tamoxifen (to 6 eugonadal men) did not affect basal plasma levels of LH, FSH, 17 alpha-hydroxyprogesterone (17-OHP), testosterone (T) and E2, whereas long-term (3 months) tamoxifen with treatment of 6 normogonadotrophic oligozoospermic men increased LH and T levels, indicating a biological effect of tamoxifen. The response of 17-OHP, T, E2 and the 17-OHP/T ratio to hCG was similar in short-term and long-term tamoxifen-treated men as well as in 6 untreated eugonadal male controls. These results do not suggest a role for endogenous E2 in the hCG-induced testicular steroidogenic block.
D000328:Adult; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D006801:Humans; D008297:Male; D009845:Oligospermia / Q000378:metabolism; D013256:Steroids / Q000096:biosynthesis*; D013268:Stimulation, Chemical; D013629:Tamoxifen / Q000494:pharmacology*; D013737:Testis / Q000378:metabolism*; D013997:Time Factors
D006063:Chorionic Gonadotropin; D013256:Steroids; D013629:Tamoxifen