Clomiphene citrate ameliorated lead acetate-induced reproductive toxicity in male Wistar rats

Objective: The current study investigated the effects of clomiphene citrate on the hypothalamic-pituitary-testicular axis, steroidogenesis, sperm parameters, and testicular antioxidant enzyme activity of male Wistar rats submitted to lead acetate (Pb)-induced reproductive toxicity. Methods: Twenty adult male Wistar rats were divided into four groups of equal size as follows: Control; Clomid (0.35 mg/kg); Pb (10 mg/kg); and Clomid + Pb. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone, testicular 17-beta hydroxysteroid dehydrogenase (17-beta HSD) activity, androgen receptors, catalase activity, superoxide dismutase (SOD), malondialdehyde (MDA), sperm motility, viability, counts and morphology were estimated after oral administration of Clomid and/or lead acetate for 35 consecutive days. Data were analyzed using ANOVA at p<0.05. Results: Lead acetate significantly decreased (p<0.05) serum LH and testosterone levels, testicular 17 beta-HSD activity, androgen receptor expression, sperm motility, viability, counts, catalase activity, and SOD when compared with controls. Abnormal sperm morphology and MDA were significantly increased (p<0.05) in the Pb group compared with controls. Clomid co-administrated with lead acetate significantly increased (p<0.05) serum LH, testosterone levels, testicular 17 beta-HSD, androgen receptor expression, sperm motility and viability when compared with the group given lead acetate. Conclusions: The present study suggests that clomiphene citrate may stimulate testicular testosterone synthesis, sperm motility and viability via luteinizing hormone in a context of lead acetate-induced reproductive toxicity.