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-β hydroxysteroid dehydrogenase
(17-β 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 17β-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 17β-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.