Copper(II)-induced Cytotoxicity and Oxidative Stress in Human Blood Cells and its Attenuation by Carnosine

Copper (Cu) is widely present in environment, mainly in +1 and +2 oxidation states. Exposure to excess Cu has adverse effects on human health. Cu toxicity is thought to be mediated through oxidative stress. The protective effect of carnosine, a dipeptide with antioxidant and antiglycating properties, against Cu(II) induced cytotoxicity was examined. Human erythrocytes and lymphocytes were incubated with 0.5 mM CuCl 2 for 1 h in presence and absence of carnosine. Cell lysates were prepared and analyzed for several parameters. Treatment of cells with CuCl 2 elevated carbonyl content, lipid peroxidation and methemoglobin levels and decreased glutathione. Impaired antioxidant power and increased formation of reactive oxygen species were observed. The activities of major antioxidant enzymes were prominently altered. The plasma membrane redox system (PMRS) of erythrocytes was inhibited and there was substantial change in membrane morphology. Preincubation of cells with carnosine attenuated the oxidative damage induced by CuCl 2 , restored the enzyme activities and antioxidant power and also prevented inactivation of erythrocyte PMRS. Carnosine protected human erythrocytes and lymphocytes from CuCl 2 -induced oxidative damage. It fortified the enzymatic and non-enzymatic antioxidant systems of these cells. The protection by carnosine can be attributed to its antioxidant nature.