Comparative protective actions of gonadotrophins and testosterone against the antispermatogenic action of ethane dimethanesulphonate

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Abstract
After a single dose of ethane dimethanesulfonate (EDS) (75 mg/kg) to rats the prolonged antispermatogenic action was due to a temporary elimination of the functional Leydig cell population. Replacement therapy with testosterone propionate (3 mg/day) maintained the spermatogenic epithelium but the EDS effect developed when hormone treatment was discontinued. In contrast, a short treatment with hCG [human chorionic gonadotropin] (10-100 I.U./day) or LH [luteinizing hormone] (714 .mu.g/day), starting before the EDS dose, permanently protected the spermatogenic epithelium. FSH treatment was completely ineffective. Although histological protection of spermatogenesis appeared complete with testosterone or hCG, effects on fertility remained but over different periods of time. Antiserpmatogenic and antifertility effects were produced in mice using much higher doses of EDS (5 .times. 250 mg/kg) but there was no protection from androgen or hCG. EDS apparently binds to Leydig cells irreversibly, interfering with the action of gonadotropin. At the dose level used the evidence suggests that the degree of reaction renders most of the Leydig cell population non-viable. A direct cytotoxic effect of the compound upon the spermatogenic epithelium might account for the inability of testosterone or hCG alone or in combination to maintain fertility at normal levels.