Ameliorative effect of L-carnitine on chronic lead-induced reproductive toxicity in male rats

Lead toxicity is one of the causative agents of male infertility that raised concern from environmental contamination worldwide. L-carnitine, a biologically active amino acid, present in high concentration in the reproductive organs such as the epididymis, is involved in sperm maturation. The possible protective effect of L-carnitine in experimentally lead-induced male reproductive toxicity in rats was evaluated in this study. Thirty adult male Wistar rats were divided into three groups. Group 1: the negative control group was treated with normal saline; Group 2: exposed to 50 mg/kg lead acetate (2% solution in saline); and Group 3: treated with lead acetate 50 mg/kg (2% solution in saline) + L-carnitine 100 mg/kg. At the end of the experimental period, body and testicular weights were determined, blood samples were withdrawn for hormonal assays of FSH, LH and testosterone. Sperm parameters as sperm count, morphology, viability and motility were measured. Testicular tissue homogenates were prepared for enzymatic assays and for measuring oxidative stress parameters. Lead significantly increased both oxidative stress and the concentration of lactate dehydrogenase-C in the testicular tissues with a decrease in sperm count, motility and viability. Lead acetate treatment, induced alteration in sperms with normal morphology together with reductions in the serum FSH, LH, testosterone, body and testicular weights. The concentration of 17 beta-hydroxysteroid dehydrogenase was significantly reduced. Co-administration of L-carnitine significantly reduced testicular oxidative stress, improved sperm parameters, elevated serum FSH, LH and testosterone with an insignificant reduction in the testicular weight. The concentrations of 17 beta-hydroxysteroid dehydrogenase and lactate dehydrogenase-C were significantly improved by L-carnitine. The overall results indicate that L-carnitine is expected to improve the lead acetate-induced male reproductive toxicity.