Effects of co-exposure to lead and zinc on redox status, kidney variables, and histopathology in adult albino rats.

Lead (Pb) is a toxic metal that induces a wide range of biochemical and physiological effects in humans. Oxidative damage has been proposed as a possible mechanism involved in Pb toxicity. The current study was carried out to evaluate the antioxidant activities of zinc (Zn) supplement against lead acetate-induced kidney injury in rats. In this study, adults male rats were treated for 15 days with Pb (0.344 g/kg body weight (bw)) associated or not with Zn (10 mg/kg bw). Our study showed that supplementation with Zn prevented renal dysfunction as indicated by plasma biomarkers (urea, uric acid, creatinine, lactate dehydrogenase, and alkaline phosphatase levels) and oxidative stress-related parameters (thiobarbituric acid reactive substances, protein carbonyl, advanced oxidation protein product, superoxide dismutase, catalase, glutathione peroxidase, and vitamins (A, E)) in kidney tissue. The corrective effect of Zn on Pb-induced kidney nephrotoxicity recovered normal kidney histology. Overall, this study indicates that Zn alleviated the toxic effects of this heavy metal on renal tissue, suggesting its role as a potential antioxidant and nephroprotective agent.