Graphical abstractA schematic diagram showing the protective effects of omega-3 fatty acids in diclofenac sodium − induced hepatotoxicity.

These results showed that hypoglycemic effects of MOLE might be mediated through the stimulation of insulin release leading to enhanced glucose uptake and glycogen synthesis.

This study further showed the gonadotoxic effect of C. sativa, which could be mediated by oxidative stress. It also showed that melatonin and vitamin C exacerbate C. sativa-induced testicular damage when administered separately but ameliorate it when combined in rats.

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Highlights The toxic effects of diclofenac (DF) seemed to be sustained after withdrawal. DF appeared to be more toxic post-administration. Melatonin could attenuate the toxic effects of DF.

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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