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Causal relationship between hexachlorocyclohexane cytotoxicity, oxidative stress and Na+, K +-ATPase in Ehrlich Ascites tumor cells.

Srivastava, Anup and Shivanandappa, T. (2006) Causal relationship between hexachlorocyclohexane cytotoxicity, oxidative stress and Na+, K +-ATPase in Ehrlich Ascites tumor cells. Molecular and Cellular Biochemistry, 286 (1-2). pp. 87-93. ISSN 0300-8177

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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.

Item Type: Article
Uncontrolled Keywords: hexachlorocyclohexane, lipid peroxidation, reactive oxygen species, Na+, K+-ATPase, antioxidants
Subjects: 600 Technology > 01 Medical sciences > 17 Toxicology
600 Technology > 08 Food technology > 32 Antioxidants
Divisions: Food Protectants and Infestation Control
Depositing User: Food Sci. & Technol. Information Services
Date Deposited: 02 Jul 2009 09:11
Last Modified: 17 Oct 2018 06:49
URI: http://ir.cftri.com/id/eprint/1949

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