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 At the end of the experimental period, body and testicular weights were determined, blood samples were withdrawn for hormonal assays of FSH, LH and testosterone.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 17β-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 17β-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.

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The main bioactive constituents in the standardized Ginkgo biloba leaf extract (EGb 761) are the terpene lactones and flavonoid glycosides. EGb 761’s antioxidant and anti-inflammatory properties have previously been demonstrated. Indomethacin-induced gastric ulcers have a multifactorial etiology and represent a major restriction to its therapeutic utility. The underlying ulcerogenic process involves oxidative and inflammatory biomolecular insults. This study was performed to explore the curative and preventative benefits of EGb 761 in experimentally-induced ulcers. To develop gastric ulcers in mice, indomethacin (40 mg/kg) was administered orally. EGb 761 (200 mg/kg) was given by gavage for 7 days before (preventative) and after (therapeutic) indomethacin administration. The histological alterations and macroscopic mucosal lesions were assessed. In gastric tissue homogenates, malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO), and inflammatory cytokines were measured. The expressions of cyclooxygenase-2 (COX-2), cytokines, and proliferating cell nuclear antigen (PCNA) in the stomach mucosa were also investigated. The ulcer index, histological alterations, gastric oxidants, and inflammatory biomarkers were all significantly increased by indomethacin. In stomach specimens, it increased COX-2 and PCNA expression. EGb 761 treatments, both prophylactic and therapeutic, resulted in significant reductions in ulcer lesions, nitrosative and oxidative damage, and inflammatory markers, along with the lowering of COX-2 and PCNA expressions. Furthermore, in the fight against stomach ulcers, EGb 761 treatment was found to be more efficient than prevention.

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