PMID: 11907164Mar 22, 2002Paper

Adenovirus-mediated overexpression of catalase in the cytosolic or mitochondrial compartment protects against toxicity caused by glutathione depletion in HepG2 cells expressing CYP2E1

The Journal of Pharmacology and Experimental Therapeutics
M MaríA I Cederbaum

Abstract

Induction of cytochrome P450 CYP2E1 by ethanol appears to be one of the mechanisms by which ethanol creates a state of oxidative stress. Glutathione (GSH) is a key cellular antioxidant that detoxifies reactive oxygen species. Depletion of GSH, especially mitochondrial GSH, is believed to play a role in the ethanol-induced liver injury. Previous results reported that depletion of GSH by buthionine-(S,R)-sulfoximine (BSO) treatment caused apoptosis and necrosis in HepG2 cells, which overexpress CYP2E1. In the current work, adenoviral infection with vectors that resulted in expression of catalase either in the cytosol or mitochondrial compartments was able to abolish the loss of mitochondrial membrane potential or damage to mitochondria observed in HepG2 cells overexpressing CYP2E1 that were treated with BSO. Loss of cell viability, either necrotic or apoptotic, was also prevented by the catalase overexpression after infection with the adenoviral vectors. The protective effects of catalase were associated with the suppression of the increase in the production of reactive oxygen species and of mitochondrial lipid peroxidation observed after GSH depletion. These results reveal a prominent role for H(2)O(2) as a mediator in the cytot...Continue Reading

References

Oct 1, 1992·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·T CastilloH Tsukamoto
Jan 1, 1992·Free Radical Biology & Medicine·R NordmannH Rouach
Oct 17, 1968·European Journal of Biochemistry·W G Niehaus, B Samuelsson
Jan 1, 1984·Recent Developments in Alcoholism : an Official Publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism·E R Gordon
Jul 1, 1995·The Journal of Clinical Investigation·H TsukamotoG M Brittenham
Jul 17, 1995·Biochimica Et Biophysica Acta·M Zoratti, I Szabò
Nov 1, 1994·Proceedings of the Society for Experimental Biology and Medicine·M MorimotoS W French
Sep 13, 1994·Proceedings of the National Academy of Sciences of the United States of America·A J BettF L Graham
Nov 1, 1993·Alcohol·J C Fernández-ChecaN Kaplowitz
Sep 27, 1996·The Journal of Biological Chemistry·D Wu, A I Cederbaum
Apr 1, 1997·Physiological Reviews·C S Lieber
May 9, 1998·Molecular Pharmacology·Q Chen, A I Cederbaum
May 15, 1998·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·C FangM Ingelman-Sundberg
Sep 29, 1999·Advances in Experimental Medicine and Biology·A G Hall
Mar 7, 2001·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·M Marí, A I Cederbaum
May 1, 2001·Alcoholism, Clinical and Experimental Research·D Wu, A I Cederbaum
May 15, 2001·Biological Signals and Receptors·C C Cunningham, S M Bailey

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Citations

May 19, 2009·Archives of Toxicology·Arthur I CederbaumDefeng Wu
Dec 17, 2003·Kidney International·Xiaoming ZhouAnupam Agarwal
Jan 28, 2004·Annual Review of Pharmacology and Toxicology·Andres A Caro, Arthur I Cederbaum
Jul 26, 2006·Expert Opinion on Drug Metabolism & Toxicology·Jose M Jimenez-Lopez, Arthur I Cederbaum
Aug 13, 2009·Expert Opinion on Drug Metabolism & Toxicology·Arthur Cederbaum
Nov 24, 2004·Drug Metabolism Reviews·Regine KahlYvonni Chovolou
Dec 3, 2009·Journal of Controlled Release : Official Journal of the Controlled Release Society·Masahiro UshitoraHiroyuki Mizuguchi
Dec 24, 2005·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Pengfei Gong, Arthur I Cederbaum
Jul 11, 2006·Life Sciences·Araní Casillas-RamírezCarmen Peralta
Jun 7, 2013·Free Radical Research·M Elias-MiróC Peralta
Apr 17, 2007·European Journal of Pharmacology·Ghanshyam UpadhyayMahendra Pratap Singh
Dec 29, 2005·The Journal of Biological Chemistry·Jingxiang Bai, Arthur I Cederbaum

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