4.7 Article

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

期刊

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
卷 24, 期 2, 页码 1898-1909

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-016-7980-7

关键词

Erythrocytes; Chlorate; Methemoglobin; Reactive oxygen species; Oxidative stress; Herbicide; Antioxidant power

资金

  1. University Grants Commission (SAP-DRS-III)
  2. UGC [201011-MANF-MUS-WES-1902]

向作者/读者索取更多资源

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 A degrees 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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