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Melatonin (Mel) is known to prevent and mitigate lead (Pb)-induced gonadotoxicity. However, there is no report in literature on the endogenous levels of different biomarkers after the cessation of Pb exposure, with or without treatment with Mel. Fifty adult male Wistar rats were divided into five groups ( N = 10), which included control ((vehicle (normal saline) - treated) − 0.1 ml/day); lead chloride (PbCl2) untreated (3 weeks vehicle + 3 weeks Pb); Pb recovery (3 weeks Pb + 3 weeks vehicle); Pb + Mel (3 weeks Pb + 3 weeks Mel); and Mel (3 weeks vehicle + 3 weeks Mel) groups. Pb and Mel were administered at 50 and 10 mg/kg B.W. ( p.o.), respectively. The results showed that Pb caused significant decreases in total bilirubin (TB), phospholipids (PLP), superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC), but significant elevations in alkaline phosphatase (ALP), aspartate aminotransferase (AST), triglyceride (TG), and malondialdehyde (MDA). Although the adverse effects of Pb on TB, ALP, AST, SOD, MDA, and TAC were sustained after the cessation of exposure, a reversal was observed in total cholesterol (TC), TG, PLP, CAT, and c-reactive protein (CRP) results. Nevertheless, the detrimental effects of Pb on alanine aminotransferase (ALT), albumin, and globulin were only expressed post-exposure. Treatment with Mel caused no significant effect on TB and albumin levels. However, unlike TAC and CRP, the hormone significantly reduced ALP, AST, ALT, TC, low-density lipoprotein cholesterol, PLP, SOD, CAT, MDA, and globulin to levels comparable to the control group. In conclusion, following the cessation of Pb exposure, alterations in physiological balance could be elevated, sustained, or reversible. However, Mel enhanced the reestablishment homeostatic status after Pb administration.

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.