Endosulfan upregulates AP-1 binding and ARE-mediated transcription via ERK1/2 and p38 activation in HepG2 cells
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TL;DR: Treatment of HepG2 cells with endosulfan significantly increased oxidative stress-responsive transcription via AP-1 activation and transcription was enhanced in cells depleted of glutathione by buthionine sulfoximine (BSO) treatment, suggesting a model for endos sulfuran toxicity in which endosolfan increases ERK1/2 and p38 activities and these activated MAPKs then increase c-Jun phosphorylation.
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About: This article is published in Toxicology. The article was published on 06 Feb 2012. and is currently open access. The article focuses on the topics: Endosulfan & Buthionine sulfoximine.
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Toxicity and Residues of Endosulfan Isomers
TL;DR: Property suggest that the alpha-isomer contributes more significantly to the residue problems associated with the insecticide than the beta-isomers and that the use of a beta-enriched insecticide would reduce residue problems yet retain the advantages to IPM and resistant management strategies unique to the current endosulfan formulation.
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TL;DR: The oxidant stress-inducing effects of endosulfan, a chlorinated hydrocarbon insecticide of the cyclodiene group, have been examined following administration of single and repeated doses and the possible relationship between the neurotoxicity and its oxidant Stress-inducing effect was discussed.
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