Control of spermatogenesis in primate and prospect of male contraception

The present review is a summary of mechanisms of spermatogenesis in primates with emphasis on anti-spermatogenesis of testosterone (T), gossypol, and "testicular heat stress" for development of male contraception, Both FSH and testosterone stimulate all phases of spermatogenesis. FSH is capable of amplifying the population of the differential spermatogonia (B1, B2, B3 and B4) and controls the spermatogonia production rate, and, in synergy with testosterone, regulating spermatogenesis in adult monkeys. Pituitary FSH beta gene expression is governed by a feedback of Beta inhibin, which is a major component of the testicular negative feedback signals. Beta inhibin secreted by Sertoli cells is in turn inhibited by testosterone from Leydig cells under the control of LH. Disturbance of the normal interaction of pituitary FSH with Sertoli cell Beta inhibin is responsible for azoospermia or oligozoospermia induced by exogenous T. Three possible regimens of T, gossypol and "heat stress" have been suggested for male contraception. They act on different sites and stages of spermatogenesis in testis or sperm activity in epididymis. Apoptosis induced by testosterone occurs mainly at staged VII-VIII of spermatogenesis while that by testicular "heat stress" mostly occurs at stages I-IV and X-XII. Low dose of gossypol mainly influences the sperm activity in the epididymis although it also acts on testicular spermatids.