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.