The Influence of Pharmaceutical Compounds on Male Fertility*

Jan 1, 1976Andrologia

How Medicines May Affect Male Fertility

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Abstract

Steroid hormones may affect spermatogenesis and fertility through various mechanisms.

All antigonadotropically active steroids inhibit spermatogenesis by reducing gonadotropin secretion.
High doses of androgens and testosterone synthesis steroids can promote spermatogenesis, but achieving necessary intratesticular levels has not been clinically feasible.
Estrogens and synthetic gestagens do not directly inhibit spermatogenesis at the testicular level; their effects can be counteracted with gonadotropins or androgens.
Only antiandrogens with antigonadotropic properties, such as cyproterone acetate, significantly inhibit spermatogenesis, while pure antiandrogens have minimal and temporary effects.
Other agents affecting spermatogenesis include certain drugs and compounds that inhibit gonadotropin secretion or damage Sertoli cells.
Contraception in men could potentially be managed with various combinations of androgens and other hormone types, but challenges remain in achieving effective methods.

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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.

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The Influence of Pharmaceutical Compounds on Male Fertility*

Abstract

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