The direct effects of estradiol (E2) and enclomiphene citrate on testicular LH/hCG receptor content, steroidogenesis and morphology were studied in immature, hypophysectomized rats treated with FSH. Treatment with FSH (100 µg bovine FSH for 5 days) caused a marked increase in testis weight. This increase was abolished by concomitant injections of E2 (1 or 10 µg), while concomitant treatment with enclomiphene citrate (1–100 µg) had no significant effect. The spermatogenesis maintained by FSH was inhibited by concomitant daily treatment with E2 (1 or 10µ g) or enclomiphene citrate (100 µg). FSH treatment increased the LH/hCG receptor content of the testis. Concomitant administration of E2 (1 or 10 µg) or a high dose of enclomiphene citrate (100 µg) abolished the FSH-induced increase in LH/hCG receptors. In vitro incubations of the testis demonstrated that FSH treatment caused a marked rise in basal and hCG-stimulated testosterone production whereas concomitant treatment with E2 or enclomiphene citrate inhibited the FSH stimulated increase in testosterone production. The steroidogenic responsiveness to hCG was markedly depressed by treatment with either 1 or 10 µg E2 (71 and 91% decreases, respectively). Likewise, treatment with 1 or 100 µg enclomiphene citrate decreased testosterone production by 32 and 60%, respectively. Associated with the decrease in testosterone production, marked suppression of androstenedione and dehydroepiandrosterone (DHEA) production was observed in animals treated with estradiol or enclomiphene citrate while that of the 17α-hydroxylated precursors was less severely affected. These steroidogenic changes were accompanied by accumulation of C2 1, steroid intermediates (progesterone and pregnenolone) suggesting that the inhibitory effect of E2 and enclomiphene citrate was associated with a defect in 17α-hydroxylase and/or 17–20 desmolase activity. The results of this study indicate that enclomiphene citrate, like E2, has a direct inhibitory effect on the testis. Low doses of these compounds inhibit testosterone production mediated via decreased steroidogenic enzyme activity, whereas high doses of these compounds further decrease testicular LH/hCG receptor content and spermatogenesis.
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Wang et al. (1980) studied this question.