Sodium chlorate, a herbicide and major water disinfectant byproduct, generates reactive oxygen species and induces oxidative damage in human erythrocytes

Abstract

Sodium chlorate (NaClO₃) is a widely used non-selective herbicide. It is also generated as a byproduct during disinfection of drinking water by chlorine dioxide. In the present work, the effects of NaClO₃ on human erythrocytes were studied under in vitro conditions. Incubation of erythrocytes with different concentrations of NaClO₃ at 37 °C for 90 min resulted in significant hemolysis. Cell lysates were prepared from NaClO₃-treated and untreated (control) erythrocytes and assayed for various biochemical parameters. Methemoglobin levels were significantly increased and methemoglobin reductase activity was reduced upon NaClO₃ treatment. There was a significant increase in protein oxidation and lipid peroxidation with a decrease in reduced glutathione and total sulfhydryl content. This suggests the induction of oxidative stress in erythrocytes upon exposure to NaClO₃. The occurrence of oxidative stress was confirmed by significantly increased generation of reactive oxygen species and lowered antioxidant response of the cells. NaClO₃ treatment also increased nitric oxide levels showing induction of nitrosative stress. The activities of major antioxidant and membrane-bound and metabolic enzymes were significantly altered upon incubation of erythrocytes with NaClO₃. The erythrocytes became more osmotically fragile while electron microscopic images showed gross morphological alterations in NaClO₃-treated cells. These results show that NaClO₃ induces oxidative stress in human erythrocytes, which results in extensive membrane damage and lowers the antioxidant response.

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