The present study aimed to investigate the histopathological and physiological effects of aluminum chloride (AlCl₃) toxicity on the liver and kidneys of mice. Hepatorenal injury was induced through oral administration of AlCl₃. Twenty-eight male Mus musculus mice were randomly divided into four groups (7 mice per group). The control group received deionized water, while the experimental groups were administered AlCl₃ at doses of 150, 200, and 300 mg/kg body weight, respectively, for a period of 30 days. Blood samples were collected 24 hours after the final dose for serum biochemical analysis, and liver and kidney tissues were subjected to histopathological examination. Histological analysis of liver tissue revealed an increased number of Kupffer cells, hepatocellular necrosis, bile duct damage, central vein congestion, endothelial hyperplasia, apoptosis, thickening of the plasma membrane, and karyorrhexis. Examination of kidney tissue showed vascular congestion, hemorrhage, glomerular atrophy and hypertrophy, hyaline necrosis, amyloid deposits, eosinophilic material accumulation, tubular necrosis and dilation, epithelial cell desquamation, and damage to Bowman’s capsule. Biochemical analysis showed a significant increase in serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine in the AlCl₃-treated groups compared to the control group. In conclusion, this study demonstrates that aluminum chloride induces significant, dose-dependent histopathological and physiological alterations in the liver and kidneys of mice, highlighting its potential toxicity to vital organs.
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