- Ameliorative effect of curcumin against lead acetate-induced hemato-biochemical alterations, hepatotoxicity, and testicular oxidative damage in rats.
Ameliorative effect of curcumin against lead acetate-induced hemato-biochemical alterations, hepatotoxicity, and testicular oxidative damage in rats.
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.