ZINC OXIDE NANOPARTICLES AMELIORATE ALUMINUM CHLORIDE-INDUCED HEPATO-RENAL OXIDATIVE STRESS AND INFLAMMATION IN RATS

Objective: The present study was designed to evaluate the effect of zinc oxide nanoparticles (ZnO NPs) on Aluminum chloride (AlCl3)-induced hepato-renal injury.  Methods: Animals were divided into, I-control group; rats received saline, II-AlCl3 group; animals received 100 mg AlCl3/kg body weight, III-ZnO NPs group; rats received 10 mg ZnO NPs/kg body weight, and IV group ZnO NPs+AlCl3. All rats were administered their respective doses daily for 6 w. Hepatorenal function parameters in sera; aminotransferases, bilirubin, urea, and creatinine were estimated. Lipid peroxide level and nitrite\nitrate ratio, glutathione content, glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase activities and interleukin-1β, tumor necrosis factor-α levels were determined in both tissues. The histopathological and the immunohistochemical investigations of nuclear factor-kB expression were carried out.  Results: ZnO NPs treatment to AlCl3-intoxicated rats significantly reduced Al accumulation (at p<0.05) in the hepatorenal tissue and increased zinc accumulation (at p<0.05) in liver and kidney, respectively, with respect to AlCl3-group, thus inhibiting oxidative stress and inflammation parameters represented by lipid peroxidation and nitric oxide levels (at p<0.05) compared to AlCl3 group and elevated antioxidant parameters (at p<0.05), compared to AlCl3 treated group, while suppressed interleukin-1β, tumor necrosis factor-α levels (at p<0.05) and the nuclear factor-kB activation in liver and kidney, especially in the kidney if compared to AlCl3-treated group. Hepatorenal function indices indicated significant decreases compared to AlCl3 group (at p<0.05). Conclusion: Results indicated the ameliorative effect of ZnO NPs on aluminum-induced hepato-renal damage.