1. Steroid hormones can affect spermatogenesis and thereby fertility directly and/or indirectly. All antigonadotropically active steroids inhibit spermatogenesis via inhibition of gonadotropin secretion, mainly that of H. Androgens and steroids occurring in the biosynthetic chain of testosterone synthesis have a direct promoting effect on spermatogenesis if applied in high doses. It has not been possible as yet to make clinical use of this positive effect since it is obviously not possible to achieve the necessary intratesticular androgen concentrations. 2. As concerns the different androgens and the steroids in the androgen biosynthetic chain, and also all synthetic anabolics, there is no parallelism between the direct spermatogenic activity, the androgenic activity and the antigonadotropic activity. 3. Estrogens and synthetic gestagens do not inhibit spermatogenesis directly at the testicular level. All effects of estrogens can be abolished experimentally by adequate substitution with gonadotropins or androgens, or a combination of androgens and gonadotropins. 4. Only those antiandrogens inhibit spermatogenesis with additional antigonadotropic properties (e.g. cyproterone acetate). Pure antiandrogens, like flutamide or cyproterone, have a slight and transient influence on spermatogenesis at the most. If at all, they merely cause transient subfertility. 5. Beside steroids and several centrally active pharmaceutics (e.g. psychotropic drugs and several antihypertensive compounds), only siloxanes and methallibur seem to affect spermatogenesis via inhibition of gonadotropin secretion. Other antispermatogenic agents act by inhibition of mitosis (Colchicine, alkylating agents) or presumably via damage of the Sertoli cells. 6. Based on present knowledge, contraception in men could be principally managed by administration of a) androgens alone, b) gestagen/androgen combinations, c) estrogen/androgen combinations, d) certain antiandrogens. 7. The difficulties of contraception in men by steroid hormones or steroid hormone combinations have been pointed out. As regards the usefulness of antiandrogens for contraception, no definite conclusions can be drawn at the moment. All non-steroidal inhibitors of spermatogenesis which have been found up to the present are not suitable because of toxic effects.
PIP: Literature on the actions of pharmaceutical compounds on testicular function and fertility is reviewed. Antigonadotropin steroids inhibit spermatogenesis by inhibiting the secretion of gonadotropins, especially luteinizing hormone. Although androgens and steroids occurring during the biosynthesis of testosterone have a positive effects on spermatogenesis in high doses, their clinical application is not yet possible because of the high intratesticular concentrations required. A parallelism between the direct spermatogenic activity, androgenic activity, and antigonadotropic activity of the various androgens and steroids occurring during androgen biosynthesis and synthetic anabolics has yet to be demonstrated. The evidence indicates that estrogens and synthetic gestagens do not affect spermatogenesis at the testicular level. Adequate doses of androgens or gonadotropins, alone or in combination, can counter the effects of estrogens on spermatogenesis. Only those antiandrogens with additional antigonadotropic properties, such as cyproterone acetate, inhibit spermatogenesi Pure antiandrogens, such as flutamide or cyproterone, cause, at most, only transient subfertility. Among psychotropic and antihypertensive compounds, only siloxanes and methallibur appear to affect spermatogenesis by inhibition of gonadotropin secretion, whereas colchicine and alkylating agents act by inhibition of mitosis, and presumably damage, of the Sertoli cells. Prospects for male hormonal contraception included the use of androgens alone, in combination with either gestagens or estrogens, and the use of some antiandrogens. So far, all nonsteroidal inhibitors of spermatogenesis investigated are not suitable for human application because of toxic effects.