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Relationship between oxidative stress and hepatic glutathione levels in ethanol-mediated apoptosis of polarized hepatic cells

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World journal of Gastroenterology 2009年第21期15卷 2609-2616页

作者： Benita L McVicker Pamela L tuma Kusum K Kharbanda Serene ML Lee dean j tuma Liver Study Unit Department of Veterans Affairs Medical Center and Department of Internal Medicine and Biochemistry & Molecular Biology University of Nebraska Medical Center Department of Biology The Catholic University of America Department of Internal Medicine and Biochemistry & Molecular Biology University of Nebraska Medical Center

AIM:To investigate the role of reactive oxygen species(ROS) in ethanol-mediated cell death of polarized hepatic(WIF-B) ***:In this work,WIF-B cultures were treated with pyrazole(inducer of cytochrome P4502E1,CYP2E1) and/or L-buthionine sulfoximine(BSO),a known inhibitor of hepatic glutathione(GSH),followed by evaluation of ROS production,antioxidant levels,and measures of cell injury(apoptosis and necrosis).RESULTS:The results revealed that ethanol treatment alone caused a significant two-fold increase in the activation of caspase-3 as well as a similar doubling in *** the activity of the CYP2E1 was increased by pyrazole pretreatment,an additional two-fold elevation in ROS was ***,the CYP2E1-related ROS elevation was not accompanied with a correlative increase in apoptotic cell injury,but rather was found to be associated with an increase in necrotic cell ***,when the thiol status of the cells was manipulated using BSO,the ethanol-induced activation of caspase-3 was ***,ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 ***:Apoptotic cell death induced as a consequence of ethanol metabolism is not completely dependent upon ROS status but is dependent on sustained GSH levels.

关键词： Fas介导乙醇处理细胞凋亡谷胱甘肽肝细胞氧化应激 caspase 极化

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Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury

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World journal of Gastroenterology 2016年第38期22卷 8497-8508页

作者： Natalia A Osna Dan Feng Murali Ganesan Priya F Maillacheruvu David j Orlicky Samuel W French dean j tuma Kusum K Kharbanda Research Service Veterans Affairs Nebraska-Western Iowa Health Care System Department of Internal Medicine 982000 Nebraska Medical Center Department of Pathology University of Colorado Denver Department of Anatomic Pathology Harbor UCLA Medical Center Department of Biochemistry and Molecular Biology 985870 Nebraska Medical Center

AIM To investigate the hypothesis that exposure to guanidinoacetate(GAA, a potent methyl-group consumer) either alone or combined with ethanol intake for a prolonged period of time would cause more advanced liver pathology thus identifying methylation defects as the initiator and stimulator for progressive liver *** Adult male Wistar rats were fed the control or ethanolLieber De Carli diet in the absence or presence of GAA supplementation. At the end of 6 wk of the feeding regimen, various biochemical and histological analyses were conducted. RESULTS Contrary to our expectations, we observed that GAA treatment alone resulted in a histologically normal liver without evidence of hepatosteatosis despite persistence of some abnormal biochemical parameters. This protection could result from the generation of creatine from the ingested GAA. Ethanol treatment for 6 wk exhibited changes in liver methionine metabolism and persistence of histological and biochemical defects as reported before. Further, when the rats were fed the GAA-supplemented ethanol diet, similar histological and biochemical changes as observed after 2 wk of combined treatment, including inflammation, macroand micro-vesicular steatosis and a marked decrease in the methylation index were noted. In addition, rats on the combined treatment exhibited increased liver toxicity and even early fibrotic changes in a subset of animals in this group. The worsening liver pathology could be related to the profound reduction in the hepatic methylation index, an increased accumulation of GAA and the inability of creatine generated to exert its hepato-protective effects in the setting of *** To conclude, prolonged exposure to a methyl consumer superimposed on chronic ethanol consumption causes persistent and pronounced liver damage.

关键词： Methyl balance S-adenosylmethionine S-adenosylhomocysteine Guanidinoacetate Alcohol

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Effect of ethanol on pro-apoptotic mechanisms in polarizedhepatic cells

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World journal of Gastroenterology 2007年第37期13卷 4960-4966页

作者： Benita L McVicker dean j tuma Carol A Casey Liver Study Unit Department of Veterans Affairs Medical Center and Departments of Internal Medicine and Biochemistry & Molecular Biology University of Nebraska Medical Center Omaha NE 68105 United States

Chronic ethanol consumption is associated with serious and potentially fatal alcohol-related liver injuries such as hepatomegaly, alcoholic hepatitis and cirrhosis. Moreover, it has been documented that the clinical progression of alcohol-induced liver damage may be associated with an increase in hepatocellular death that involves apoptotic mechanisms. Although much information has been learned about the clinical manifestations associated with alcohol-related diseases, the search continues for a better understanding of the molecular and/or cellular mechanisms by which ethanol exerts its deleterious effects such as the induction of pro-apoptotic mechanisms and related cell damaging events. As part of the effort to enhance our understanding of those particular cellular pathways and mechanisms associated with ethanol toxicity, researchers over the years have utilized a variety of model systems. Recently, work has come forth demonstrating the utility of a hybrid cell line (WIF-B) as a cell culture model system for the study of alcohol-associated alterations in hepatocellular mechanisms. Success with such emerging model systems could aid in the development of potential therapeutic treatments for the prevention of alcohol- induced apoptotic cell death that may ultimately serve as a significant target in delaying the onset and/or progression of clinical symptoms of alcohol-mediated liver disease. This review article summarizes the current understanding of ethanol-mediated modifications in cell survival and thus the promotion of pro-apoptotic events with emphasis on analyses made in various experimental model systems, particularly the more recently characterized WIF-B cell system.

关键词：肝细胞肝癌细胞酒精细胞凋亡

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