LAUSR

Lead, toxic heavy metal of global concern, induces toxicity in various organs via oxidative stress. Thereby, in this study, the protective role of curcumin against lead acetate-induced toxicity was evaluated. Thirty-two male albino rats were allocated equally into four groups and orally administered with corn oil as a vehicle (Cont.), curcumin (CUR) (400 mg/kg bw), lead acetate (LA) (100 mg/kg bw), and lead acetate plus curcumin (LA + CUR). All rats had received their treatments daily for 4 weeks. The results revealed that LA toxicity induced normocytic normochromic anemia with significant leukocytosis and lymphocytosis. Moreover, LA-intoxicated rats showed a marked elevation in the liver enzyme activities, serum cholesterol, and triglyceride levels. In contrast, sero-immunological parameters, total protein, albumin, globulin, and testosterone levels were significantly reduced compared to the control rats. Additionally, LA-induced hepatic and testicular oxidative damage revealed by marked increased in MDA level with prominent reduction in the antioxidant system. The gene expression of the hepatic pro-inflammatory markers and testicular steroidogenic biomarkers including LHR and aromatase were significantly upregulated; meanwhile, the expressions of testicular StAR, CYP17a, 3B-HDS, SR-B1, and P450SCC were significantly downregulated in the LA-intoxicated group. Curcumin treatment could partially improve the hematological, biochemical, and histopathological alterations induced by LA. Also, it was observed that curcumin significantly restored hepatic pro-inflammatory markers and testicular steroidogenic enzymes. In conclusion, curcumin has antioxidant, anti-inflammatory, and immunomodulatory effects and is able to minimize the LA-induced oxidative damage in rats.