Subacute exposure to aluminium chloride induces cytotoxicity and oxidative stress in rat erythrocytes: a dose-dependent study

Aluminium (Al) toxicity has attracted considerable interest due to its bioavailability, environmental persistence, and adverse health effects. The present study investigates the effect of Al on rat erythrocytes under in vivo conditions. Rats were administered 0 (control), 25 (Al 1), 35 (Al 2), 45 (Al 3), and 55 (Al 4) mg/kg b.wt. of AlCl₃ orally for 30 days. Hemolysates were prepared from different experimental groups and assayed for various biochemical parameters. AlCl₃ administration significantly increased protein oxidation and lipid peroxidation, while decreasing total sulfhydryl and glutathione levels in rat erythrocytes. Methemoglobin level was increased and methemoglobin reductase activity was decreased upon AlCl₃ treatment. Prolonged AlCl₃ exposure inhibited the activities of antioxidant enzymes, and lowered the cells' antioxidant power. It also caused an increase in H₂O₂ and NO levels showing generation of oxidative and nitrosative stress. AlCl₃ intoxication adversely affected the membrane-bound and metabolic enzyme activities. Alterations in all the biochemical parameters were found in an AlCl₃ dose-dependent manner. Scanning electron microscopy showed gross morphological changes in erythrocytes from discocytes to acanthocytes and echinocytes, further supporting the damaging effect of aluminium. The aluminium-induced oxidative stress seems to be the key mechanism of damage to the cellular components that could lead to red cell senescence.