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Green tea polyphenol epigallocatechin-3-gallate protects HepG2 cells against CYP2E1-dependent toxicity.
Free Radic Biol Med. 2004 Feb 01; 36(3):359-70.FR

Abstract

Chronic ethanol consumption causes oxidative damage in the liver, and induction of cytochrome P450 2E1 (CYP2E1) is one pathway involved in oxidative stress produced by ethanol. The hepatic accumulation of iron and polyunsaturated fatty acids significantly contributes to ethanol hepatotoxicity in the intragastric infusion model of ethanol treatment. The objective of this study was to analyze the effect of the green tea flavanol epigallocatechin-3-gallate (EGCG), which has been shown to prevent alcohol-induced liver damage, on CYP2E1-mediated toxicity in HepG2 cells overexpressing CYP2E1 (E47 cells). Treatment of E47 cells with arachidonic acid plus iron (AA + Fe) was previously reported to produce synergistic toxicity in E47 cells by a mechanism dependent on CYP2E1 activity and involving oxidative stress and lipid peroxidation. EGCG protected E47 cells against toxicity and loss of viability induced by AA+Fe; EGCG had no effect on CYP2E1 activity. Prevention of this toxicity was associated with a reduction in oxidative damage as reflected by decreased generation of reactive oxygen species, a decrease in lipid peroxidation, and maintenance of intracellular glutathione in cells challenged by AA+Fe in the presence of EGCG. AA+Fe treatment caused a decline in the mitochondrial membrane potential, which was also blocked by EGCG. In conclusion, EGCG exerts a protective action on CYP2E1-dependent oxidative stress and toxicity that may contribute to preventing alcohol-induced liver injury, and may be useful in preventing toxicity by various hepatotoxins activated by CYP2E1 to reactive intermediates.

Authors+Show Affiliations

Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, NY 10029, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15036355

Citation

Jimenez-Lopez, Jose M., and Arthur I. Cederbaum. "Green Tea Polyphenol Epigallocatechin-3-gallate Protects HepG2 Cells Against CYP2E1-dependent Toxicity." Free Radical Biology & Medicine, vol. 36, no. 3, 2004, pp. 359-70.
Jimenez-Lopez JM, Cederbaum AI. Green tea polyphenol epigallocatechin-3-gallate protects HepG2 cells against CYP2E1-dependent toxicity. Free Radic Biol Med. 2004;36(3):359-70.
Jimenez-Lopez, J. M., & Cederbaum, A. I. (2004). Green tea polyphenol epigallocatechin-3-gallate protects HepG2 cells against CYP2E1-dependent toxicity. Free Radical Biology & Medicine, 36(3), 359-70.
Jimenez-Lopez JM, Cederbaum AI. Green Tea Polyphenol Epigallocatechin-3-gallate Protects HepG2 Cells Against CYP2E1-dependent Toxicity. Free Radic Biol Med. 2004 Feb 1;36(3):359-70. PubMed PMID: 15036355.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Green tea polyphenol epigallocatechin-3-gallate protects HepG2 cells against CYP2E1-dependent toxicity. AU - Jimenez-Lopez,Jose M, AU - Cederbaum,Arthur I, PY - 2003/08/04/received PY - 2003/11/07/revised PY - 2003/11/20/accepted PY - 2004/3/24/pubmed PY - 2004/10/16/medline PY - 2004/3/24/entrez SP - 359 EP - 70 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 36 IS - 3 N2 - Chronic ethanol consumption causes oxidative damage in the liver, and induction of cytochrome P450 2E1 (CYP2E1) is one pathway involved in oxidative stress produced by ethanol. The hepatic accumulation of iron and polyunsaturated fatty acids significantly contributes to ethanol hepatotoxicity in the intragastric infusion model of ethanol treatment. The objective of this study was to analyze the effect of the green tea flavanol epigallocatechin-3-gallate (EGCG), which has been shown to prevent alcohol-induced liver damage, on CYP2E1-mediated toxicity in HepG2 cells overexpressing CYP2E1 (E47 cells). Treatment of E47 cells with arachidonic acid plus iron (AA + Fe) was previously reported to produce synergistic toxicity in E47 cells by a mechanism dependent on CYP2E1 activity and involving oxidative stress and lipid peroxidation. EGCG protected E47 cells against toxicity and loss of viability induced by AA+Fe; EGCG had no effect on CYP2E1 activity. Prevention of this toxicity was associated with a reduction in oxidative damage as reflected by decreased generation of reactive oxygen species, a decrease in lipid peroxidation, and maintenance of intracellular glutathione in cells challenged by AA+Fe in the presence of EGCG. AA+Fe treatment caused a decline in the mitochondrial membrane potential, which was also blocked by EGCG. In conclusion, EGCG exerts a protective action on CYP2E1-dependent oxidative stress and toxicity that may contribute to preventing alcohol-induced liver injury, and may be useful in preventing toxicity by various hepatotoxins activated by CYP2E1 to reactive intermediates. SN - 0891-5849 UR - https://www.unboundmedicine.com/medline/citation/15036355/Green_tea_polyphenol_epigallocatechin_3_gallate_protects_HepG2_cells_against_CYP2E1_dependent_toxicity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891584903007925 DB - PRIME DP - Unbound Medicine ER -