20 - World Journal of Gastroenterology

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cytotoxic activity in chronic alcoholism is associated with alcohol liver disease but not active ethanol consumption. Hepatology 1997; 25: 1096-1100 96 Szabo G, Mandrekar P, Girouard L, Catalano D. Regulation of human monocyte functions by acute ethanol treatment: decreased tumor necrosis factor-alpha, interleukin-1 beta and elevated interleukin-10, and transforming growth factor-beta production. Alcohol Clin Exp Res 1996; 20: 900-907 97 Jaruga B, Hong F, Kim WH, Sun R, Fan S, Gao B. Chronic alcohol consumption accelerates liver injury in T cell-mediated hepatitis: alcohol disregulation of NF-kappaB and STAT3 signaling pathways. Am J Physiol Gastrointest Liver Physiol 2004; 287: G471-G479 98 Minagawa M, Deng Q, Liu ZX, Tsukamoto H, Dennert G. Activated natural killer T cells induce liver injury by Fas and tumor necrosis factor-alpha during alcohol consumption. Gastroenterology 2004; 126: 1387-1399 99 Pianko S, Patella S, Ostapowicz G, Desmond P, Sievert W. Fas-mediated hepatocyte apoptosis is increased by hepatitis C virus infection and alcohol consumption, and may be associated with hepatic fibrosis: mechanisms of liver cell injury in chronic hepatitis C virus infection. J Viral Hepat 2001; 8: 406-413 100 Rigamonti C, Mottaran E, Reale E, Rolla R, Cipriani V, Capelli F, Boldorini R, Vidali M, Sartori M, Albano E. Moderate alcohol consumption increases oxidative stress in patients with chronic hepatitis C. Hepatology 2003; 38: 42-49 101 Bataller R, Paik YH, Lindquist JN, Lemasters JJ, Brenner DA. Hepatitis C virus core and nonstructural proteins induce fibrogenic effects in hepatic stellate cells. Gastroenterology 2004; WJG|www.wjgnet.com Suh YG et al . HSCs and innate immunity in liver disease 126: 529-540 102 Machida K, Cheng KT, Sung VM, Levine AM, Foung S, Lai MM. Hepatitis C virus induces toll-like receptor 4 expression, leading to enhanced production of beta interferon and interleukin-6. J Virol 2006; 80: 866-874 103 Barnes PJ, Karin M. Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases. N Engl J Med 1997; 336: 1066-1071 104 Spahr L, Rubbia-Brandt L, Pugin J, Giostra E, Frossard JL, Borisch B, Hadengue A. Rapid changes in alcoholic hepatitis histology under steroids: correlation with soluble intercellular adhesion molecule-1 in hepatic venous blood. J Hepatol 2001; 35: 582-589 105 Taïeb J, Mathurin P, Elbim C, Cluzel P, Arce-Vicioso M, Bernard B, Opolon P, Gougerot-Pocidalo MA, Poynard T, Chollet-Martin S. Blood neutrophil functions and cytokine release in severe alcoholic hepatitis: effect of corticosteroids. J Hepatol 2000; 32: 579-586 106 Akriviadis E, Botla R, Briggs W, Han S, Reynolds T, Shakil O. Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial. Gastroenterology 2000; 119: 1637-1648 107 Mezey E, Potter JJ, Rennie-Tankersley L, Caballeria J, Pares A. A randomized placebo controlled trial of vitamin E for alcoholic hepatitis. J Hepatol 2004; 40: 40-46 108 Parés A, Planas R, Torres M, Caballería J, Viver JM, Acero D, Panés J, Rigau J, Santos J, Rodés J. Effects of silymarin in alcoholic patients with cirrhosis of the liver: results of a controlled, double-blind, randomized and multicenter trial. J Hepatol 1998; 28: 615-621 S- Editor Tian L L- Editor Stewart GJ E- Editor Zheng XM 2551 May 28, 2011|Volume 17|Issue 20|
Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v17.i20.2552 Natalia A Osna, MD, PhD, Series Editor Role of MGST1 in reactive intermediate-induced injury Courtney S Schaffert Courtney S Schaffert, Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198-5870, United States Author contributions: Schaffert CS solely contributed to this review. Correspondence to: Courtney S Schaffert, PhD, Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198-5870, United States. cschaffert@unmc.edu Telephone: +1-402-5596647 Fax: +1-402-5596650 Received: March 17, 2011 Revised: April 15, 2011 Accepted: April 22, 2011 Published online: May 28, 2011 Abstract Microsomal glutathione transferase (MGST1, EC 2.5.1.18) is a membrane bound glutathione transferase extensively studied for its ability to detoxify reactive intermediates, including metabolic electrophile intermediates and lipophilic hydroperoxides through its glutathione dependent transferase and peroxidase activities. It is expressed in high amounts in the liver, located both in the endoplasmic reticulum and the inner and outer mitochondrial membranes. This enzyme is activated by oxidative stress. Binding of GSH and modification of cysteine 49 (the oxidative stress sensor) has been shown to increase activation and induce conformational changes in the enzyme. These changes have either been shown to enhance the protective effect ascribed to this enzyme or have been shown to contribute to cell death through mitochondrial permeability transition pore formation. The purpose of this review is to elucidate how one enzyme found in two places in the cell subjected to the same conditions of oxidative stress could both help protect against and contribute to reactive oxygen species-induced liver injury. © 2011 Baishideng. All rights reserved. Key words: Microsomal glutathione transferase 1; Oxidative stress; Mitochondrial permeability transition; Glutathione; Liver injury WJG|www.wjgnet.com 2552 World J Gastroenterol 2011 May 28; 17(20): 2552-2557 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2011 Baishideng. All rights reserved. Peer reviewers: Vasiliy I Reshetnyak, MD, PhD, Professor, Scientist Secretary of the Scientific Research Institute of General Reanimatology, 25-2, Petrovka str., 107031, Moscow, Russia; Jay Pravda, MD, Inflammatory Disease Research Center, Gainesville, FL 32614-2181, United States Schaffert CS. Role of MGST1 in reactive intermediate-induced injury. World J Gastroenterol 2011; 17(20): 2552-2557 Available from: URL: http://www.wjgnet.com/1007-9327/full/v17/ i20/2552.htm DOI: http://dx.doi.org/10.3748/wjg.v17.i20.2552 INTRODUCTION TOPIC HIGHLIGHT Tissue damage due to excessive production of reactive intermediates (reactive oxygen species (ROS), reactive nitrogen species (RNS), lipid peroxides, free radicals) has been shown to be a major part of various pathologies including atherosclerosis, diabetes, cancer, ischemia-reperfusion injury, aging, and liver injury from both alcoholic and non-alcoholic origins [1-3] . Organisms have evolved many defense mechanisms as protection from these reactive intermediates. These include, but aren’t limited to, various enzymes such as superoxide dismutase, Se-dependent glutathione peroxidase, catalase, glutaredoxins, peroxiredoxins, and glutathione transferases (GSTs) [4] . GSTs bind and conjugate electrophiles to GSH to, in effect, neutralize them, and protect the cells. Some GSTs also have glutathione peroxidase activities. While many GSTs are cytosolic, other GSTs exist that are integral membrane proteins. They are members of the membrane associated proteins in eicosanoid and glutathione metabolism (MAPEG) family, which include enzymes that synthesize prostaglandins and leukotrienes. Microsomal glutathione transferase 1 (MGST1) is a member of this family and is the subject of the following review. MGST1 STRUCTURE AND FUNCTION MGST1 is an approximately 17 kDa membrane bound glutathione s-transferase [5] . It is found in the highest May 28, 2011|Volume 17|Issue 20|
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S Contents EDITORIAL TOPIC HIGHLIGH
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Contents APPENDIX FLYLEAF EDITORS F
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