Copper(II) generates ROS and RNS, impairs antioxidant system and damages membrane and DNA in human blood cells.

Abstract

Copper (Cu) is widely used in various industries, and human exposure to this metal results in severe multi-organ toxicity, which is thought to be due to the generation of free radicals by Fenton-like reaction. The generation of reactive oxygen as well as nitrogen species and free radicals results in induction of oxidative stress in the cell. We have studied the effect of different concentrations of Cu(II) on human erythrocytes and lymphocytes. Incubation of erythrocytes with copper chloride, a Cu(II) compound, enhanced the production of reactive oxygen and nitrogen species, decreased glutathione and total sulphydryl content and increased protein oxidation and lipid peroxidation. All changes were in a Cu(II) concentration-dependent manner. This strongly suggests that Cu(II) causes oxidative damage in erythrocytes. The activities of major antioxidant enzymes were altered, and antioxidant power was lowered. Cu(II) treatment also resulted in membrane damage in erythrocytes as seen by electron microscopy and lowered activities of plasma membrane-bound enzymes. Incubation of human lymphocytes with Cu(II) resulted in DNA damage when studied by the sensitive comet assay. These results show that Cu(II) exerts cytotoxic and genotoxic effects on human blood cells probably by enhancing the generation of reactive oxygen and nitrogen species.