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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 | Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury显示文摘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 damage.METHODS 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 ethanol.CONCLUSION To conclude, prolonged exposure to a methyl consumer superimposed on chronic ethanol consumption causes persistent and pronounced liver damage. | Natalia A Osna Dan Feng Murali Ganesan Priya F Maillacheruvu David J Orlicky Samuel W French Dean J Tuma Kusum K Kharbanda | 2016 | World Journal of Gastroenterology2016，22，38： | 2 |
| 3 | 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 |
| 4 | Influence of marbling and animal age on factors associated with beef quality显示文摘 | Tuma H J Henrickson R L Stephens D F | 1962 | Animal Science1962，21，11： | 1 |
| 5 | Solubility of CO2 in the ionic liquid 显示文摘 | Perez-Salado Kamps A Tuma D Xia J | 2003 | Journal of Chemical & Engineering Data2003，48，3： | 1 |
| 6 | Group-47η61 -pyrrolyl complexes incorporating N, N-Di (pyrrolyl-α-methyl)-N-methylamine 显示文摘 | Li Y H Tumas A Cizewski J T | 2002 | Inorg Chem2002，41，： | 1 |
| 7 | Safety,pharmacokinetics and pharmacodynamics of GS-9620,an oral Toll-like receptor 7 agonist显示文摘 | Lopatin U Wolfgang G Tumas D Frey CR Ohmstede C Hesselgesser J Kearney B Moorehead L Subramanian G M McHutchison J G | 2013 | Antivir Ther2013，18，3： | 1 |
| 8 | Specific adsorption of some complement activation proteins to polysulfone dialysis membranes during hemodialysis显示文摘 | Mares J Thongboonkerd V Tuma Z | 2009 | Kidney Int2009，76，4： | 1 |
| 9 | Lentiviral gene transfer ameliorates disease progression in Long-Evans cinnamon rats: an animal model for Wilson disease 显示文摘 | Merle U Encke J Tuma S | 2006 | Scandinavian Journal of Gastroenterology2006，41，8： | 1 |
| 10 | 显示文摘 | Tuma R Prevelige P E Thomas G J | 1996 | Biochemistry1996，35，14： | 1 |
| 11 | Ethanol feeding inhibits the activity of hepatic N5 methyltetrahydrofolate-homocysteine methyltransferase in the rat显示文摘 | BARAK A J BECKENHAUER H C TUMA D J | 1985 | IRCS Med Sci1985，13，8： | 1 |
| 12 | Effects of prolonged ethanol feeding in methionine metabolism in rat liver显示文摘 | BARAK A J BECKENHAUER H C TUMA D J | 1987 | Biochem Cell Biol1987，65，3： | 1 |
| 13 | Solubility of CO in the ionic liquid 显示文摘 | Kumelan J Perez'Salado Kamps A Tuma D | 2005 | Fluid Phase Equil2005，，： | 1 |
| 14 | Solubility of CO2 in the ionic liquid 显示文摘 | Kamps A Tuma D Xia J Z et ol | 2003 | J Chem Eng Data2003，48，3： | 1 |
| 15 | Dangerous Byproducts of Alcohol Breakdown Focus on Adducts显示文摘 | TUMA D J CASEY C A | 2003 | Alcohol Res Health2003，27，4： | 1 |
| 16 | Microtubules are more stable and more highly acetylated in ethanol-treated he- patic cells显示文摘 | Kannarkat G T Tuma D J Tuma P L | 2006 | J Hepatol2006，44，5： | 1 |
| 17 | Solubility of CO2 in the ionic liquids and 显示文摘 | Kumelan J Perez-Salado Kamps A Tuma D | 2006 | J Chem Eng Data2006，51，5： | 1 |
| 18 | Results of reconstruction of the facial nerve显示文摘 | Ferreira M C Besteiro J M Tuma Junior P | 1994 | Microsurgery1994，15，1： | 1 |
| 19 | Relaxin reduces fibrosis in models of progressive and established hepatic fibrosis显示文摘 | BENNETT R G HEIMANN D G TUMA D J | 2009 | Ann N Y Acad Sci2009，1160，1： | 1 |
| 20 | Solubility of CO2 in the Ionic Liquid IBmiml PF61 显示文摘 | Kamps A P S Tuma D Xia J | 2003 | J Chem EngData2003，48，3： | 1 |
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