Abstract
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.
Highlights
Aluminum (Al) represents about 8% of the total mineral constituents of the earth’s crust and classified among the most harmful toxicants in the environment [1]
Rats were divided into four groups (n=7 rats in each): I-control group (CNT); animals were received oral saline daily, II-AlCl3 treated group; rats were received daily oral AlCl3 100 mg/kg body weight, III-zinc oxide nanoparticles (ZnO NPs) treated group; rats have received ZnO NPs 10 mg/kg body weight, orally, once, and in ZnO NPs+AlCl3 treated group, rats were administered 10 mg/kg of ZnO NPs one h prior to 100 mg/kg of AlCl3
In the ZnO NPs+AlCl3 group, rats pretreated with ZnO NPs (10 mg/kg) for the same period showed a marked decrease in Al accumulation as compared with AlCl3-exposed animals as illustrated in fig. 1
Summary
Aluminum (Al) represents about 8% of the total mineral constituents of the earth’s crust and classified among the most harmful toxicants in the environment [1]. Humans are exposed mainly to Al through drinking water, food additives, and packaging, cooking utensils, deodorants and medicines [2]. Al accumulates in different organs causing neurological, respiratory, immunological, skeletal and hematopoietic problems [3]. Chronic administration of Al-induced changes in the morphological structure of glomeruli and proximal tubular cells and affected the levels of kidney function parameters [6]. Oxidative stress is an important mechanism involved in Al-induced hepato-renal toxicity, through enhanced lipid peroxidation, nitric oxide formation and depressed cellular glutathione [5, 7]
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