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Potentiation of Endosulfan Induced Oxidative Stress by Thiram

Manasa, B. (2009) Potentiation of Endosulfan Induced Oxidative Stress by Thiram. [Student Project Report]

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This Dissertation / Report is the outcome of investigation carried out by the creator(s) / author(s) at the department/division of Central Food Technological Research Institute (CFTRI), Mysore mentioned below in this page.

Item Type: Student Project Report
Additional Information: The present study focuses on the potentiation of endosulfan by thiram in vivo. Thebiochemical mechanism of the pesticides viz., endosulfan and thiram alone and in theircombinations has been reported in many in vitro studies. Thiram induced cytotoxicity is accompanied by a rapid and diastic oxidation ofreduced glutathione with consecutive lipid peroxidation and cell death (Boget et al., 2001).Cytotoxicity of thiram in human and master fibroblast cells have been investigated (Cereseret al., 2001), the principle cause of cytotoxicity in fibroblasts is GSH depletion. Endosulfan induced cytotoxicity is shown by the inhibition of cellular respiration andthe recovery of respiratory activity by antioxidant treatment. This confirmed the induction ofoxidative stress and inhibition of respiration via ROS generation by Endosulfan. (Sohn et al.,2004). Cytotoxicity of the two pesticides, thiram and endosulfan, have been studied in Erlichascites tumour cells. (In vitro study by Rana and Shivanandappa, 2009). The cytotoxic action of the pesticides on the cells were characterised by glutathione depletion, induction of reactive oxygen species. The cell death induced by the pesticides was of necrotic type as confirmed by the LDH leakage. At non-cytotoxic concentration, thiram potentiated the cytotoxicity of endosulfan when cells were exposed to a mixture of both chemicals. In our study, cytotoxicity mediated by the mixture of pesticides viz., endosulfan and thiram on liver and brain is evident by ROS induction, Lipid peroxidation and Glutathione depletion. Reactive oxygen species are produced as a part of normal metabolism in the cell and its effect is counteracted by antioxidant mechanism. ROS production is found to enhance on exposure to xenobiotic leading to depletion of antioxidant level in the cell. Our study showed the increase in ROS production in liver and brain with both the doses (single and double) indicating the stress response of cells due to oxidative damage brought about by intoxication of mixture of pesticides. GSH (glutathione) is a major non-enzymatic antioxidant. It is a tripeptide (γ-glutamylcysteinylglycine) ubiquitously found in cells. The antioxidant activity of glutathione protects the cells against oxidative damage by free radicals and represents an important cellular defence mechanism. GSH pool is maintained in the cells by the restoration of oxidised form of glutathione (GSSH). In the presence of xenobiotics GSH levels gets depleted indicating the detoxifying mechanism of GSH dependent reaction (Robert and Orrenius, 2000). Our findings, showed GSH depletion in liver and brain with both the doses indicating higher oxidative stress brought about by mixture of both the pesticides. LPO damage leads to membrane dysfunction and covalent binding of reactive intermediates formed during the toxication reactions. Our study, showed a marked increase in LPO with mixtures of pesticides in liver and brain with both the doses indicating higher lipid peroxidation due to membrane damage and dysfunction.
Uncontrolled Keywords: Thiram, dithiocarbamate fungicide; harvested crops protection; Organochlorine pesticides
Subjects: 600 Technology > 03 Agriculture > 05 Insect/Pest Control
Divisions: Food Protectants and Infestation Control
Depositing User: Food Sci. & Technol. Information Services
Date Deposited: 28 Jun 2010 04:06
Last Modified: 28 Dec 2011 10:14
URI: http://ir.cftri.com/id/eprint/9432

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