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Updated: Aug 13, 2026

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents (HPHC)
Published on: May 10, 2016
Causal relationship between hexachlorocyclohexane cytotoxicity, oxidative stress and Na+, K +-ATPase in Ehrlich
Anup Srivastava1, T Shivanandappa
1Department of Food Protectants and Infestation Control, Central Food Technological Research Institute, Mysore 570020, India. anup_s100@yahoo.com
Abstract:
Role of oxidative stress and Na+,K+-ATPase in the cytotoxicity of hexachlorocyclohexane (HCH) on Ehrlich Ascites tumor (EAT) cells has been studied. HCH caused dose dependent cell death as measured by trypan blue exclusion and lactate dehydrogenase (LDH) leakage from the cells. HCH induced oxidative stress in EAT cells which was characterized by glutathione depletion, lipid peroxidation (LPO), reactive oxygen species (ROS) production and inhibition of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT). Protective effect of antioxidants on HCH induced oxidative stress was assessed, among the antioxidants used only quercetin inhibited HCH-induced LPO and ROS production as well as cell death whereas alpha -tocopherol, ascorbic acid and BHA inhibited LPO but not cell death. Inhibition of membrane bound Na+,K+-ATPase was a characteristic feature of HCH cytotoxicity in EAT cells. Experimental evidence indicates that HCH-induced cell death involves oxidative stress due to ROS production and membrane perturbation in EAT cells.
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