20 - World Journal of Gastroenterology

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38 He Y, Wang J, Liu X, Zhang L, Yi G, Li C, He X, Wang P, Jiang H. Toosendanin inhibits hepatocellular carcinoma cells by inducing mitochondria-dependent apoptosis. Planta Med 2010; 76: 1447-1453 39 Lu C, Armstrong JS. Role of calcium and cyclophilin D in the regulation of mitochondrial permeabilization induced by glutathione depletion. Biochem Biophys Res Commun 2007; 363: 572-577 40 Palmeira CM, Wallace KB. Benzoquinone inhibits the voltage-dependent induction of the mitochondrial permeability transition caused by redox-cycling naphthoquinones. Toxicol Appl Pharmacol 1997; 143: 338-347 41 Yang L, Liu X, Lu Z, Yuet-Wa Chan J, Zhou L, Fung KP, Wu P, Wu S. Ursolic acid induces doxorubicin-resistant HepG2 cell death via the release of apoptosis-inducing factor. Cancer Lett 2010; 298: 128-138 42 He L, Lemasters JJ. Regulated and unregulated mitochondrial permeability transition pores: a new paradigm of pore structure and function? FEBS Lett 2002; 512: 1-7 43 Ulziikhishig E, Lee KK, Hossain QS, Higa Y, Imaizumi N, WJG|www.wjgnet.com Schaffert CS et al . MGST1: Friend or foe? Aniya Y. Inhibition of mitochondrial membrane boundglutathione transferase by mitochondrial permeability transition inhibitors including cyclosporin A. Life Sci 2010; 86: 726-732 44 Schaffert C, Duryee M, Hunter C, Kreikemeier C, Tuma D, Thiele G, Klassen L. Detection and Activation of Malondialdehyde-Acetaldehyde (MAA)-Adducted Microsomal Glutathione S-Transferase 1 (MGST1) Following Chronic Ethanol Feeding. Hepatology 2010; 52: 320A-421A 45 Tuma DJ, Thiele GM, Xu D, Klassen LW, Sorrell MF. Acetaldehyde and malondialdehyde react together to generate distinct protein adducts in the liver during long-term ethanol administration. Hepatology 1996; 23: 872-880 46 Xu D, Thiele GM, Kearley ML, Haugen MD, Klassen LW, Sorrell MF, Tuma DJ. Epitope characterization of malondialdehyde-acetaldehyde adducts using an enzyme-linked immunosorbent assay. Chem Res Toxicol 1997; 10: 978-986 47 Xiong Q, Hase K, Tezuka Y, Namba T, Kadota S. Acteoside inhibits apoptosis in D-galactosamine and lipopolysaccharide-induced liver injury. Life Sci 1999; 65: 421-430 S- Editor Tian L L- Editor Rutherford A E- Editor Ma WH 2557 May 28, 2011|Volume 17|Issue 20|
Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v17.i20.2558 Natalia A Osna, MD, PhD, Series Editor Proteasome inhibitor treatment in alcoholic liver disease Fawzia Bardag-Gorce Fawzia Bardag-Gorce, Department of Pathology, Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, 1124 W. Carson St., Torrance, CA 90502, United States Author contributions: Bardag-Gorce F wrote this review. Supported by NIH/NIAAA 8116 and by a Pilot Project Funding from the Alcohol Center Grant on Liver and Pancreas P50-011999 Correspondence to: Fawzia Bardag-Gorce, PhD, Department of Pathology, Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, 1124 W. Carson St., Torrance, CA 90502, United States. fgorce@labiomed.org Telephone: +1-310-2221846 Fax: +1-310-2223614 Received: January 6, 2011 Revised: February 2, 2011 Accepted: February 9, 2011 Published online: May 28, 2011 Abstract Oxidative stress, generated by chronic ethanol consumption, is a major cause of hepatotoxicity and liver injury. Increased production of oxygen-derived free radicals due to ethanol metabolism by CYP2E1 is principally located in the cytoplasm and in the mitochondria, which does not only injure liver cells, but also other vital organs, such as the heart and the brain. Therefore, there is a need for better treatment to enhance the antioxidant response elements. To date, there is no established treatment to attenuate high levels of oxidative stress in the liver of alcoholic patients. To block this oxidative stress, proteasome inhibitor treatment has been found to significantly enhance the antioxidant response elements of hepatocytes exposed to ethanol. Recent studies have shown in an experimental model of alcoholic liver disease that proteasome inhibitor treatment at low dose has cytoprotective effects against ethanol-induced oxidative stress and liver steatosis. The beneficial effects of proteasome inhibitor treatment against oxidative stress occurred because antioxidant response elements (glutathione peroxidase 2, superoxide dismutase 2, glutathione synthetase, glutathione reductase, and GCLC) were upregulated when rats fed alcohol were treated with a low dose of PS-341 (Bortezomib, Velcade ® ). This is an WJG|www.wjgnet.com World J Gastroenterol 2011 May 28; 17(20): 2558-2562 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2011 Baishideng. All rights reserved. important finding because proteasome inhibitor treatment up-regulated reactive oxygen species removal and glutathione recycling enzymes, while ethanol feeding alone down-regulated these antioxidant elements. For the first time, it was shown that proteasome inhibition by a highly specific and reversible inhibitor is different from the chronic ethanol feeding-induced proteasome inhibition. As previously shown by our group, chronic ethanol feeding causes a complex dysfunction in the ubiquitin proteasome pathway, which affects the proteasome system, as well as the ubiquitination system. The beneficial effects of proteasome inhibitor treatment in alcoholic liver disease are related to proteasome inhibitor reversibility and the rebound of proteasome activity 72 h post PS-341 administration. © 2011 Baishideng. All rights reserved. Key words: Alcoholic liver disease; Glutathione; Oxidative stress; Proteasome inhibitor treatment; Steatosis Peer reviewer: Saúl Villa-Trevio, MD, PhD, Departamento de Biología Celular, Centro de Investigación y de Estudios Avanzados del IPN (Cinvestav), Ave. IPN No. 2508. Col. San Pedro, Zacatenco, CP 07360, México, DF, Mexico Bardag-Gorce F. Proteasome inhibitor treatment in alcoholic liver disease. World J Gastroenterol 2011; 17(20): 2558-2562 Available from: URL: http://www.wjgnet.com/1007-9327/full/v17/i20/ 2558.htm DOI: http://dx.doi.org/10.3748/wjg.v17.i20.2558 INTRODUCTION TOPIC HIGHLIGHT Excessive alcohol consumption is recognized worldwide as a leading cause of disease, disability, and death [1] . Alcoholic liver disease (ALD) is a collective term for the pathophysiological changes caused by chronic alcohol consumption. These changes include oxidative stress generation, liver steatosis and inflammatory response fibrosis, and cirrhosis. 2558 May 28, 2011|Volume 17|Issue 20|
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Italy Donato F Altomare, Bari Piero
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