Toxicology and Industrial Health · 2018 · 32 citations · 26 references
PharmacyEndocrinologyToxicologyEnvironmental ToxicologyReproductive EndocrinologyReproductive ToxicologyGonadal HormonesHeavy Metal Reproductive ToxicityLead ExposureLead ToxicologyMale Reproductive ToxicologyTesticular FunctionEnvironmental Chemical GonadotoxicityGonadotoxicity MechanismsHeavy Metal GonadotoxicityLead Reproductive ToxicityLead Toxicity MechanismsMelatonin TreatmentOxidative Stress InjuryTesticular Oxidative Damage
We investigated the effects of melatonin on sperm parameters and some biochemical markers in lead-exposed male Wistar rats. Lead (50 mg/kg bw/day) and/or melatonin (4 mg/kg or 10 mg/kg bw/day) was administered for 4 weeks, while 2-week lead exposure was preceded by or followed by 2-week treatment with both doses of melatonin in other groups. Lead reduced glutathione, catalase, adjusted testes weight, semen parameters but did not change malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, and total antioxidant capacity. Though independent of prolactin, lead-induced gonadotoxicity was both centrally and peripherally mediated, as it reduced gonadotropin-releasing hormone and testosterone levels, while gonadotropin levels did not change significantly probably due to negative feedback by elevated estradiol. However, pre-, simultaneous, or posttreatment of lead-exposed rats with melatonin reduced MDA, SOD, and estradiol but dose-dependently increased other parameters. Conclusively, lead causes male gonadotoxicity through oxidative stress and endocrine mechanisms, and these could be dose-dependently prevented and ameliorated by melatonin.
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