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| 1 | Relationship between oxidative stress and hepatic glutathione levels in ethanol-mediated apoptosis of polarized hepatic cells显示文摘AIM:To investigate the role of reactive oxygen species(ROS) in ethanol-mediated cell death of polarized hepatic(WIF-B) cells.METHODS: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 ROS.When the activity of the CYP2E1 was increased by pyrazole pretreatment,an additional two-fold elevation in ROS was detected.However,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 death.Interestingly,when the thiol status of the cells was manipulated using BSO,the ethanol-induced activation of caspase-3 was abrogated.Additionally,ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.CONCLUSION:Apoptotic cell death induced as a consequence of ethanol metabolism is not completely dependent upon ROS status but is dependent on sustained GSH levels. | Benita L McVicker Pamela L Tuma Kusum K Kharbanda Serene ML Lee Dean J Tuma | 2009 | World Journal of Gastroenterology2009，15，21： | 5 |
| 2 | Effect of ethanol on pro-apoptotic mechanisms in polarizedhepatic cells显示文摘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. | Benita L McVicker Dean J Tuma Carol A Casey | 2007 | World Journal of Gastroenterology2007，13，37： | 2 |
| 3 | Proteomics reveal a concerted upregulation of methionine metabolic pathway enzymes, and downregulation of carbonic anhydrase-III, in betaine supplemented ethanol-fed rats显示文摘 | Kusum K. Kharbanda Vasanthy Vigneswara Benita L. McVicker Anna U. Newlaczyl Kevin Bailey Dean Tuma David E. Ray Wayne G. Carter | 2009 | Biochemical and Biophysical Research Communications2009，，4： | 2 |
| 4 | Impact of asialoglycoprotein receptor deficiency on the development of liver injury显示文摘The asialoglycoprotein (ASGP) receptor is a wellcharacterized hepatic receptor that is recycled via the common cellular process of receptor-mediated endocytosis (RME). The RME process plays an integral part in the proper traff icking and routing of receptors and ligands in the healthy cell. Thus, the missorting or altered transport of proteins during RME is thought to play a role in several diseases associated with hepatocyte and liver dysfunction. Previously, we examined in detail alterations that occur in hepatocellular RME and associated receptor functions as a result of one particular liver injury, alcoholic liver disease (ALD). The studies revealed profound ethanolmediated impairments to the ASGP receptor and the RME process, indicating the importance of this receptor and the maintenance of proper endocytic events in normal tissue. To further clarify these observations, studies were performed utilizing knockout mice (lacking a functional ASGP receptor) to which were administered several liver toxicants. In addition to alcohol, we examined the effects following administration of antiFas (CD95) antibody, carbon tetrachloride (CCl4) and lipopolysaccharide (LPS)/galactosamine. The results of these studies demonstrated that the knockout mice sustained enhanced liver injury in response to all of the treatments, as shown by increased indices of liver damage, such as enhancement of serum enzyme levels, histopathological scores, as well as hepatocellular death. Overall, the work completed to date suggests a possible link between hepatic receptors and liver injury. In particular, adequate function and content of the ASGP receptor may provide protection against various toxinmediated liver diseases. | Serene ML Lee Carol A Casey Benita L McVicker | 2009 | World Journal of Gastroenterology2009，15，10： | 2 |
| 5 | Cellular fi bronectin stimulates hepatocytes to produce factors that promote alcohol-induced liver injury显示文摘AIM:To examine the consequences of cellular f ibronectin(cFn)accumulation during alcohol-induced injury,and inv estigate whether increased cFn could have an effect on hepatocytes(HCs)by producing factors that could cont ribute to alcohol-induced liver injury.METHODS:HCs were isolated from rats fed a control or ethanol liquid diet for four to six weeks.Exogenous c Fn(up to 7.5 μg/mL)was added to cells cultured for 20 h,and viability(lactate dehydrogenase),apoptosis(caspase activity)and se cretion of proinflammat-ory cytokines(tumor ne c rosis fac tor alpha,TNF-α and interleukin 6,IL-6),mat rix metalloproteinases(MMPs)and their inhibitors(tissue inhibitors of metall-oproteinases,TIMPs)was det ermined.Degrad ation of iodinated cFn was det ermined over a 3 h time period in the preparations.RESULTS:cFn degradation is impaired in HCs isolated from ethanol-fed animals,leading to its accumulation in the matrix.Addition of exogenous cFn did not affect viability of HCs from control or ethanolfed animals,and apoptosis was affected only at the higher concentration.Sec retion of MMPs,TIMPs,TNF-α and IL-6,however,was increased by exogenously added cFn,with HCs from ethanolfed animals showing increased susceptibility compared to the controls.CONCLUSION:These results suggest that the elevated amounts of cFn observed in alcoholic liver injury can stimulate hepatocytes to produce factors which promote further tissue damage. | Razia S Aziz-Seible Benita L McVicker Kusum K Kharbanda Carol A Casey | 2011 | World Journal of Hepatology2011，3，2： | 2 |
| 6 | Hydrogenation of polystyrene in CO2-expanded liquids: The effect of catalyst composition on deactivation显示文摘 | Dong L B McVicker G B Kiserow D J | 2010 | Applied Catalysis 4: General2010，384，12： | 1 |
| 7 | Preparation of Bulk and Supported Heteropoly Acid Salts显示文摘 | Soled S Miseo S Mcvicker G | 1997 | Ca-talysis Today1997，36，4： | 1 |
| 8 | Isolation and character-ization of the P5 adhesin protein of Haemophilus pa-rasuis serotype 5显示文摘 | McVicker J K Tabatabai L B | 2006 | Prep Biochem Biotechnoi2006，36，： | 1 |
| 9 | Preparation and catalytic properties of supported heteropoly acid salts 显示文摘 | Soled S Miseo S Mcvicker G | 1996 | The Chemical Engineering Journal1996，64，： | 1 |
| 10 | Repeated allergen inhalation induces cytoskeletal remodeling in smooth muscle from rat bronchioles 显示文摘 | McVicker CG Leung SY Kanabar V | 2007 | Am J Respir Cell Mol Biol2007，36，6： | 1 |
| 11 | Selective ring opening of naphthenic molecules显示文摘 | McVicker G B Daage M Touvelle M S Hudson C W Klein D P Baird W C Cook B R Chen J G Hantzer S Vaughan D E W Ellis E S Feeley O C | | 0，，01： | 1 |
| 12 | Mechanisms of leukotriene D4-induced constriction in human small bronchioles显示文摘 | Snetkov VA Hapgood KJ McVicker CG d al | 2001 | Br J Pharmacol2001，133，2： | 1 |
| 13 | Haemophilus parasuis-novel proteins-hopes for vaccine显示文摘 | Mcvicker J Tabatabai L Muriel V S | 2005 | Respiratory Diseases of Livestock2005，10，： | 1 |
| 14 | Isolation and characterization of the P5 adhesin protein of Haemophilus parasuis serotype 5显示文摘 | Mcvicker J K Tabatabai L B | 2006 | Prep Biochem Biotechnol2006，36，4： | 1 |
| 15 | Hatmophilus parasuis-novel proteins-hopes for vaccine显示文摘 | Mcvicker J Tabatabal L Muriel V S | 2005 | Respiratory diseases of livestock2005，10，： | 1 |
| 16 | Proteomics reveal a concerted upregulation of methionine metabolic pathway enzymes,and downregulation of carbonic anhydrase-Ⅲ,in betaine supplemented ethanol-fed rats显示文摘 | Kharbandak K Vigneswara V Mcvicker B L | 2009 | Biochem Biophys Res Commun2009，381，4： | 1 |
| 17 | Selective ring opening of naphthenic molecules显示文摘 | Mcvicker G B Daage M Touvelie M S | 2002 | J Catal2002，210，1： | 1 |
| 18 | Widespread genomic signatures of natural selection in hominid evolution显示文摘 | McVicker G Gordon D Davis C | 2009 | PLoS Genetics2009，5，10： | 1 |
| 19 | Preparation of Bulk and Supported Heteropolyacid Salts显示文摘 | Soled S Miseo S Mcvicker G | 1997 | Catalysis Today1997，36，： | 1 |
| 20 | Defect structure and acid catalysis of high silica, FAU - framework zeolites: Effects of aluminum re- moval and of basic metal oxide addition 显示文摘 | Beyerlein R A McVicker G B | 2001 | Studies in Surface Science and Catalysis2001，134，： | 1 |
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