The present study was designed to evaluate the hepatotoxicity of aluminium oxide (Al2O3). To achieve this objective, Al2O3 of three different sizes (30 nm, 40 nm and bulk) was orally administered for 28 days to 9 groups of 10 Wistar rats each, at the dose of 500, 1000 and 2000 mg/Kg/rat. A tenth group of 10 rats received distilled water and served as control. After 28 days of exposure, the animals were sacrificed and the serum was collected and tested for the activity levels of aminotransferases (AST or GOT and ALT or GPT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzymes following standard testing methods. Reduced glutathione (GSH) content was also measured in the liver tissue to study the oxidative stress. A histopathological evaluation was also performed to determine the extent of liver injury. Study results indicated that the activity of both the aminotransferases (AST and ALT), ALP and LDH increased significantly in Al2O3-treated rats compared to control animals. The increase was found to be more pronounced with Al2O3-30 nm followed by Al2O3-40 nm and Al2O3-bulk-treated rats in a dose-dependent manner. However reduced glutathione content showed a decline in the activity. Ultra structural assessment showed significant morphological changes in the liver tissue in accordance with biochemical parameters. Taken together, the results of this study demonstrated that Al2O3 is hepatotoxic and the smaller size of this nanomaterial appeared to be the most toxic while the compound in the bulk form seemed to be the least toxic.
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