Research Topics
Genomes and Genes | R G ThurmanSummaryAffiliation: University of North Carolina Country: USA Publications
| Collaborators
|
Detail Information
Publications
Sex-related liver injury due to alcohol involves activation of Kupffer cells by endotoxinR G Thurman
The University of North Carolina at Chapel Hill, 27599 7365, USA
Can J Gastroenterol 14:129D-135D. 2000..These data support the hypothesis that Kupffer cells contribute to the vital sex differences in liver injury caused by ethanol...- The role of gut-derived bacterial toxins and free radicals in alcohol-induced liver injuryR G Thurman
Department of Pharmacology, The University of North Carolina at Chapel Hill, 27599 7365, USA
J Gastroenterol Hepatol 13:S39-50. 1998..Furthermore, oestrogen treatment increased the sensitivity of Kupffer cells to endotoxin. These data are consistent with the hypothesis that Kupffer cells participate in important gender differences in liver injury caused by ethanol... - Mechanisms of alcohol-induced hepatotoxicity: studies in ratsR G Thurman
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7365, USA
Front Biosci 4:e42-6. 1999..The increase in oxygen demand leads to hypoxia in the liver, and on reperfusion, alpha-hydroxyethyl free radicals are formed which lead to tissue damage in oxygen-poor pericentral regions of the liver lobule... - Overexpression of manganese superoxide dismutase prevents alcohol-induced liver injury in the ratM D Wheeler
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, 27599, USA
J Biol Chem 276:36664-72. 2001..These results also support the hypothesis that mitochondrial oxidant production is a critical factor in parenchymal cell death caused by alcohol... - Adenoviral gene delivery can inactivate Kupffer cells: role of oxidants in NF-kappaB activation and cytokine productionM D Wheeler
Laboratory of Hepatobiology and Toxicology, University of North Carolina at Chapel Hill, USA
J Leukoc Biol 69:622-30. 2001..These findings suggest that Kupffer cell-targeted approaches may be a potential therapeutic strategy against many inflammatory diseases including early alcohol-induced liver injury... - Estrogen is involved in early alcohol-induced liver injury in a rat enteral feeding modelM Yin
Laboratory of Hepatobiology and Toxicology, University of North Carolina, Chapel Hill, NC 27599 7365, USA
Hepatology 31:117-23. 2000..It is concluded, therefore, that the sensitivity of rat liver to alcohol-induced injury is directly related to estrogen, which increases endotoxin in the blood and CD14 expression in the liver, leading to increased TNF-alpha production... - Delivery of the Cu/Zn-superoxide dismutase gene with adenovirus reduces early alcohol-induced liver injury in ratsM D Wheeler
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
Gastroenterology 120:1241-50. 2001..Therefore, it was hypothesized that increased and stable expression of the antioxidant enzyme Cu/Zn-superoxide dismutase (SOD1) would diminish oxygen free radicals and reduce alcohol-induced liver injury... - The role of Kupffer cell oxidant production in early ethanol-induced liver diseaseM D Wheeler
Laboratory of Hepatobiology and Toxicology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7365, USA
Free Radic Biol Med 31:1544-9. 2001..This review highlights new data in support of the hypothesis that Kupffer cells play a pivotal role in hepatotoxicity due to ethanol by producing oxidants via NADPH oxidase... - Diphenyleneiodonium sulfate, an NADPH oxidase inhibitor, prevents early alcohol-induced liver injury in the ratH Kono
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Mary Ellen Jones Bldg, Chapel Hill, NC 27599-7365, USA
Am J Physiol Gastrointest Liver Physiol 280:G1005-12. 2001..These results indicate that DPI prevents early alcohol-induced liver injury, most likely by inhibiting free radical formation via NADPH oxidase, thereby preventing NF-kappaB activation and TNF-alpha mRNA expression in the liver... - Delivery of IkappaB superrepressor gene with adenovirus reduces early alcohol-induced liver injury in ratsT Uesugi
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, NC 27599-7365, USA
Hepatology 34:1149-57. 2001..These data support the hypothesis that NF-kappaB inhibition prevents early alcohol-induced liver injury even in the presence of oxidative stress... - Toll-like receptor 4 is involved in the mechanism of early alcohol-induced liver injury in miceT Uesugi
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, NC, USA
Hepatology 34:101-8. 2001..These data are consistent with the hypothesis that Kupffer cell activation by endotoxin via TLR4 is involved in early alcohol-induced liver injury... - Delivery of Cu/Zn-superoxide dismutase genes with a viral vector minimizes liver injury and improves survival after liver transplantation in the ratT G Lehmann
Department of Pharmacology, University of North Carolina, Chapel Hill 27599, USA
Transplantation 69:1051-7. 2000.... 
NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver diseaseH Kono
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599 7365, USA
J Clin Invest 106:867-72. 2000....- Phthalates rapidly increase production of reactive oxygen species in vivo: role of Kupffer cellsI Rusyn
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599 7365, USA
Mol Pharmacol 59:744-50. 2001..These observations represent the first direct, in vivo evidence that phthalates increase free radicals in liver before peroxisomal oxidases are induced... - Alcohol-induced free radicals in mice: direct toxicants or signaling molecules?M Yin
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Hepatology 34:935-42. 2001..These findings are consistent with the hypothesis that free radicals act as redox signals for TNF-alpha production and do not directly damage cells in early alcohol-induced hepatic injury... - ICAM-1 is involved in the mechanism of alcohol-induced liver injury: studies with knockout miceH Kono
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, NC 27599 7365, USA
Am J Physiol Gastrointest Liver Physiol 280:G1289-95. 2001..These data demonstrate that ICAM-1 and infiltrating leukocytes play important roles in early alcohol-induced liver injury, most likely by mechanisms involving TNF-alpha... - Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in ratsP Schemmer
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
Am J Physiol Gastrointest Liver Physiol 280:G1076-82. 2001..Thus modulation of Kupffer cell function before organ harvest could be beneficial in human liver transplantation and surgery... - Cu/Zn-superoxide dismutase gene attenuates ischemia-reperfusion injury in the rat kidneyM Yin
Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA
J Am Soc Nephrol 12:2691-700. 2001..In conclusion, these results indicate that SOD expression can be increased by delivery of the sod gene to the kidney by intravenous injection and that sod gene transduction minimized ischemia-reperfusion-induced acute renal failure... - Reduced early alcohol-induced liver injury in CD14-deficient miceM Yin
Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina, Chapel Hill, NC 27599, USA
J Immunol 166:4737-42. 2001..Thus, chronic ethanol feeding caused more severe liver injury in wild-type than CD14 knockouts, supporting the hypothesis that endotoxin acting via CD14 plays a major role in the development of early alcohol-induced liver injury... - Chronic ethanol increases adeno-associated viral transgene expression in rat liver via oxidant and NFkappaB-dependent mechanismsM D Wheeler
Laboratory of Hepatobiology and Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Hepatology 32:1050-9. 2000..g., superoxide dismutase). Moreover, this study has important implications for rAAV gene therapy and potential enhancement and regulation of transgene expression in liver... - Development of an animal model of chronic alcohol-induced pancreatitis in the ratH Kono
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7365, USA
Am J Physiol Gastrointest Liver Physiol 280:G1178-86. 2001..The animal model presented here is the first to demonstrate chronic alcohol-induced pancreatitis in a reproducible manner. The key factors responsible for pathology are the amount of ethanol administered and the type of dietary fat... - Long-term alcohol exposure changes sensitivity of rat Kupffer cells to lipopolysaccharideN Enomoto
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Alcohol Clin Exp Res 25:1360-7. 2001..This study was designed to elucidate the temporal effect of chronic ethanol exposure on Kupffer cell sensitization to LPS... - Dietary glycine blunts lung inflammatory cell influx following acute endotoxinM D Wheeler
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599 7365, USA
Am J Physiol Lung Cell Mol Physiol 279:L390-8. 2000..Importantly, glycine diet for 4 wk protected against lung inflammation due to endotoxin. Chronic glycine improves survival by unknown mechanisms, but reduction of lung inflammation is likely involved... - Cyclosporin A causes a hypermetabolic state and hypoxia in the liver: prevention by dietary glycineZ Zhong
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599 7365, USA
J Pharmacol Exp Ther 299:858-65. 2001..It is hypothesized that CsA activates Kupffer cells and increases production of PGE(2), which alters mitochondria leading to a hypermetabolic state. Glycine inhibits activation of Kupffer cells thus preventing liver injury... - Autonomic nervous system and gut-derived endotoxin: involvement in activation of Kupffer cells after in situ organ manipulationP Schemmer
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
World J Surg 25:399-406. 2001..These data indicate for the first time that both the autonomic nervous system and gut-derived endotoxin are involved in activation of Kupffer cells after organ manipulation... - Corn oil rapidly activates nuclear factor-kappaB in hepatic Kupffer cells by oxidant-dependent mechanismsI Rusyn
Department of Pharmacology, Department of Medicine and Department of Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, NC 27599 7365, USA
Carcinogenesis 20:2095-100. 1999..It is concluded that corn oil rapidly activates NF-kappaB in Kupffer cells via oxidant-dependent mechanisms. This triggers production of low levels of TNFalpha which is mitogenic in liver and promotes growth of hepatocytes... - Viral delivery of superoxide dismutase gene reduces cyclosporine A-induced nephrotoxicityZ Zhong
Laboratory of Hepatobiology and Toxicology, and Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill 27599-7365, USA
Kidney Int 59:1397-404. 2001..CONCLUSIONS: CsA increases free radical formation. Gene delivery of SOD blocks formation of free radicals, thereby minimizing nephrotoxicity caused by CsA... - [Preparing the donor with glycine improves survival after liver transplantation in the animal model]P Schemmer
Lab of Hepatobiology and Toxicology, Dept of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
Langenbecks Arch Chir Suppl Kongressbd 115:589-93. 1998..These data indicate for the first time that pretreatment of donors with intravenous glycine prevents the detrimental effects of graft manipulation during harvest on outcome... - Attenuation of CCl(4)-induced hepatic fibrosis by GdCl(3) treatment or dietary glycineC A Rivera
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
Am J Physiol Gastrointest Liver Physiol 281:G200-7. 2001..These results support previous in vitro data and demonstrate that treatment of rats with the selective Kupffer cell toxicant GdCl(3) prevents stellate cell activation and the development of fibrosis... - Dietary glycine prevents peptidoglycan polysaccharide-induced reactive arthritis in the rat: role for glycine-gated chloride channelX Li
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, North Carolina 27599-7365, USA
Infect Immun 69:5883-91. 2001..This work supports the hypothesis that glycine prevents reactive arthritis by blunting cytokine release from macrophages by increasing chloride influx via a glycine-gated chloride channel... - Viral gene delivery of superoxide dismutase attenuates experimental cholestasis-induced liver fibrosis in the ratZ Zhong
Department of Pharmacology, School of Medicine, University of North Carolina at Chapel Hill, NC 27599-7365, USA
Gene Ther 9:183-91. 2002..Gene delivery of mitochondrial Mn-SOD blocks formation of oxygen radicals and production of toxic cytokines thereby minimizing liver injury caused by cholestasis... - Evidence that hypoxia markers detect oxygen gradients in liver: pimonidazole and retrograde perfusion of rat liverG E Arteel
Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill 27599, USA
Br J Cancer 72:889-95. 1995..It is concluded that low oxygen concentration rather than the non-homogeneous distribution of nitroreductase activity is the primary determinant of 2-nitroimidazole binding in liver... - Comparison of the effect of adenoviral delivery of three superoxide dismutase genes against hepatic ischemia-reperfusion injuryM D Wheeler
Department of Pharmacology and Center for Alcohol Studies, CB 7365 Mary Ellen Jones Bldg, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Hum Gene Ther 12:2167-77. 2001..These data demonstrate that adenoviral delivery of superoxide dismutase can effectively reduce hepatic oxidative stress... - Gadolinium chloride-induced hepatocyte proliferation is prevented by antibodies to tumor necrosis factor alphaM L Rose
Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, 27599, USA
Toxicol Appl Pharmacol 170:39-45. 2001.... - Reperfusion injury is dramatically increased by gentle liver manipulation during harvestP Schemmer
Department of Pharmacology, University of North Carolina, Chapel Hill, USA
Transpl Int 13:S525-7. 2000..These findings demonstrate Kupffer cell-dependent reperfusion injury of sinusoidal lining cells caused by manipulation of the liver during its recovery. The mechanisms are those of proteolysis and impaired hepatic microcirculation... - Potent peroxisome proliferators inhibit beta-oxidation in the isolated perfused rat liverH K Bojes
Department of Pharmacology and Curriculum in Toxicology, University of North Carolina at Chapel Hill, 27599 7365, USA
Toxicol Appl Pharmacol 140:322-7. 1996..This phenomenona, which occurs due to inhibition of acyl CoA synthetase, leads to an elevation of free fatty acids that stimulates protein kinase C and promotes cell proliferation... - Ischemic preconditioning of rat livers against cold storage-reperfusion injury: role of nonparenchymal cells and the phenomenon of heterologous preconditioningM Arai
Department of Cell Biology and Anatomy, School of Medicine, University of North Carolina at Chapel Hill, USA
Liver Transpl 7:292-9. 2001..Moreover, ischemia to half the liver confers protection to the other half. Such heterologous preconditioning provides a new means to protect liver tissue against ischemia-reperfusion injury without imposing ischemia on the target tissue... - Essential role of tumor necrosis factor alpha in alcohol-induced liver injury in miceM Yin
Laboratory of Hepatobiology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Gastroenterology 117:942-52. 1999..To obtain clear evidence for or against the hypothesis that TNF-alpha is involved, we studied TNF receptor 1 (TNF-R1, p55) or 2 (TNF-R2, p75) knockout mice... - Food restriction and stimulation of monooxygenation of p-nitroanisole in perfused rat liverW Qu
Department of Pharmacology, University of North Carolina at Chapel Hill, 27599 7365
Biochem Pharmacol 48:311-7. 1994..This, in turn, increases the availability of reducing equivalents in the form of NADPH by a malate-pyruvate exchange system, leading to increased drug metabolism... - Oxidants from nicotinamide adenine dinucleotide phosphate oxidase are involved in triggering cell proliferation in the liver due to peroxisome proliferatorsI Rusyn
Department of Pharmacology, University of North Carolina at Chapel Hill, 27599, USA
Cancer Res 60:4798-803. 2000.... - Novel role of oxidants in the molecular mechanism of action of peroxisome proliferatorsI Rusyn
Department of Pharmacology and Curriculum in Toxicology, University of North Carolina, Chapel Hill 27599 7365, USA
Antioxid Redox Signal 2:607-21. 2000.... - Endothelial cells contain a glycine-gated chloride channelS Yamashina
Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7365, USA
Nutr Cancer 40:197-204. 2001..This hyperpolarizes the cell membrane and blocks influx of Ca2+, thereby minimizing growth factor-mediated signaling... - Gene and antisense delivery in alcoholism researchY Israel
Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Alcohol Clin Exp Res 26:582-5. 2002..Crews; (3) Gene therapy in alcoholic liver injury, by Ronald Thurman; and (4) Antisense oligonucleotides and antisense-gene delivery, by Yedy Israel...