Aluminum (Al) is a toxic metal and exposure to it in various ways is unavoidable owing to its abundant presence and use in everyday life Aluminum exposure leads to serious, lifethreatening complications as it accumulates in all tissues of mammals. Twenty four adult male albino rats were equally divided into three groups; group I was used as a negative control, group II received normal saline intraperitoneally (positive control group) and group III received Aluminum chloride (Al Cl3) intraperitoneally at 10 mg/kg body weight/day (1/ 20 of LD50) for 30 days (treated group).  At the end of the experimental period, blood was withdrawn for estimating liver and kidney functions (serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen and creatinine levels respectively). Then the rats were sacrificed and the brain, liver and kidney were examined by light microscope for detecting histopathological changes. Tissue sections were examined immunohistochemically for the detection of the caspase 3 (apoptosis-related cytosine peptidase) protein immunoreactions activity. In Al Cl3 reated group (group III), there were significant increases in serum AST, ALT, blood urea nitrogen and creatinine. Histopathological changes were in the form of: neuronal degeneration of the cerebral cortex with increased number of pyramidal cells and fibrillary background of the brain, dilated congested central vein, loss of cord arrangement of hepatocytes and lipid accumulation in the hepatocytes of the liver, and dilated swollen glomeruli with obstruction in renal tubules of the kidney. Cytoplasmic caspase 3 protein showed strong immunoreaction in neuronal cells, hepatocytes and renal tissues. On the light of the results of the present study, it can be concluded that Al Cl3 induced toxic injuries in the brain, liver and kidney as evidenced by biochemical, histopathological and immunohistochemical changes.