The administration of testosterone (T) to normal men to suppress spermatogenesis has been assessed by the World Health Organization as a reversible male contraceptive. While this approach shows promise, several problems limit its potential widespread use. Response to T treatment varies and there are adverse effects of androgen administration. A clear need exists for improved safety, acceptability and efficacy of androgen-based methods of contraception. The reasons for heterogeneity of response to T-based contraception are unclear. In humans there are only very limited qualitative descriptions of testicular histology during T treatment and no systematic data on germ cell populations or other aspects of intra-testicular physiology. The nonhuman primate model provides a bridge between lower mammals and humans; this concept is particularly relevant to male contraception because of marked differences between rodents and primates in the ability of hormonal methods to affect spermatogenesis. As our major goal is to understand human hormonal contraception, we have established a primate model of T-induced gonadotropin withdrawal so that morphological studies of testis biopsies and biochemical studies can be assessed. In this study we are assessing quantitative germ cell counts, intra-testicular T and dihydrotestosterone levels, and apoptosis in monkey testes during hormonal regimens designed to suppress spermatogenesis. The initial pilot regimen is with T alone. The results of this work will be assessed in view of the hypothesis that androgens are involved in maintaining germ cell-Sertoli cell adhesion (perhaps through cadherin), and that total androgen withdrawal leads to earlier and more complete suppression of spermatogenesis through blocking cell adhesion in addition to blocking spermatogonial replication.
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