Abstract
The aim of this study was to investigate the mechanism by which amphetamine exerts its inhibitory effect on testicular interstitial cells of male rats.
Administration of amphetamine (10−12–10−6 M) in vitro resulted in a dose-dependent inhibition of both basal and human chorionic gonadotropin (hCG, 0.05 iu ml−1)-stimulated release of testosterone.
Amphetamine (10−9 M) enhanced the basal and hCG-increased levels of adenosine 3′:5′-cyclic monophosphate (cyclic AMP) accumulation in vitro (P<0.05) in rat testicular interstitial cells.
Administration of SQ22536, an adenylyl cyclase inhibitor, decreased the basal release (P<0.05) of testosterone in vitro and abolished the inhibitory effect of amphetamine.
Nifedipine (10−6 M) alone decreased the secretion of testosterone (P<0.01) but it failed to modify the inhibitory action of amphetamine (10−10–10−6 M).
Amphetamine (10−10–10−6 M) significantly (P<0.05 or P<0.01) decreased the activities of 3β-hydroxysteroid dehydrogenase (3β-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography (t.l.c.).
These results suggest that increased cyclic AMP production, decreased Ca2+ channel activity and decreased activities of 3β-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.
Keywords: Amphetamine, testosterone, cyclic AMP, calcium, steroidogenesis
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