R G Thurman

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. ncbi request reprint Sex-related liver injury due to alcohol involves activation of Kupffer cells by endotoxin
    R G Thurman
    The University of North Carolina at Chapel Hill, 27599 7365, USA
    Can J Gastroenterol 14:129D-135D. 2000
  2. ncbi request reprint The role of gut-derived bacterial toxins and free radicals in alcohol-induced liver injury
    R G Thurman
    Department of Pharmacology, The University of North Carolina at Chapel Hill, 27599 7365, USA
    J Gastroenterol Hepatol 13:S39-50. 1998
  3. ncbi request reprint Mechanisms of alcohol-induced hepatotoxicity: studies in rats
    R 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
  4. ncbi request reprint Overexpression of manganese superoxide dismutase prevents alcohol-induced liver injury in the rat
    M 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
  5. ncbi request reprint Adenoviral gene delivery can inactivate Kupffer cells: role of oxidants in NF-kappaB activation and cytokine production
    M D Wheeler
    Laboratory of Hepatobiology and Toxicology, University of North Carolina at Chapel Hill, USA
    J Leukoc Biol 69:622-30. 2001
  6. ncbi request reprint Estrogen is involved in early alcohol-induced liver injury in a rat enteral feeding model
    M Yin
    Laboratory of Hepatobiology and Toxicology, University of North Carolina, Chapel Hill, NC 27599 7365, USA
    Hepatology 31:117-23. 2000
  7. ncbi request reprint Delivery of the Cu/Zn-superoxide dismutase gene with adenovirus reduces early alcohol-induced liver injury in rats
    M 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
  8. ncbi request reprint The role of Kupffer cell oxidant production in early ethanol-induced liver disease
    M 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
  9. ncbi request reprint Diphenyleneiodonium sulfate, an NADPH oxidase inhibitor, prevents early alcohol-induced liver injury in the rat
    H 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
  10. ncbi request reprint Delivery of IkappaB superrepressor gene with adenovirus reduces early alcohol-induced liver injury in rats
    T Uesugi
    Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina, Chapel Hill, NC 27599-7365, USA
    Hepatology 34:1149-57. 2001

Detail Information

Publications43

  1. ncbi request reprint Sex-related liver injury due to alcohol involves activation of Kupffer cells by endotoxin
    R 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...
  2. ncbi request reprint The role of gut-derived bacterial toxins and free radicals in alcohol-induced liver injury
    R 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...
  3. ncbi request reprint Mechanisms of alcohol-induced hepatotoxicity: studies in rats
    R 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...
  4. ncbi request reprint Overexpression of manganese superoxide dismutase prevents alcohol-induced liver injury in the rat
    M 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...
  5. ncbi request reprint Adenoviral gene delivery can inactivate Kupffer cells: role of oxidants in NF-kappaB activation and cytokine production
    M 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...
  6. ncbi request reprint Estrogen is involved in early alcohol-induced liver injury in a rat enteral feeding model
    M 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...
  7. ncbi request reprint Delivery of the Cu/Zn-superoxide dismutase gene with adenovirus reduces early alcohol-induced liver injury in rats
    M 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...
  8. ncbi request reprint The role of Kupffer cell oxidant production in early ethanol-induced liver disease
    M 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...
  9. ncbi request reprint Diphenyleneiodonium sulfate, an NADPH oxidase inhibitor, prevents early alcohol-induced liver injury in the rat
    H 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...
  10. ncbi request reprint Delivery of IkappaB superrepressor gene with adenovirus reduces early alcohol-induced liver injury in rats
    T 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...
  11. ncbi request reprint Toll-like receptor 4 is involved in the mechanism of early alcohol-induced liver injury in mice
    T 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...
  12. ncbi request reprint Delivery of Cu/Zn-superoxide dismutase genes with a viral vector minimizes liver injury and improves survival after liver transplantation in the rat
    T G Lehmann
    Department of Pharmacology, University of North Carolina, Chapel Hill 27599, USA
    Transplantation 69:1051-7. 2000
    ....
  13. pmc NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease
    H 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
    ....
  14. ncbi request reprint Phthalates rapidly increase production of reactive oxygen species in vivo: role of Kupffer cells
    I 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...
  15. ncbi request reprint 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...
  16. ncbi request reprint ICAM-1 is involved in the mechanism of alcohol-induced liver injury: studies with knockout mice
    H 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...
  17. ncbi request reprint Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in rats
    P 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...
  18. ncbi request reprint Cu/Zn-superoxide dismutase gene attenuates ischemia-reperfusion injury in the rat kidney
    M 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...
  19. ncbi request reprint Reduced early alcohol-induced liver injury in CD14-deficient mice
    M 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...
  20. ncbi request reprint Chronic ethanol increases adeno-associated viral transgene expression in rat liver via oxidant and NFkappaB-dependent mechanisms
    M 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...
  21. ncbi request reprint Development of an animal model of chronic alcohol-induced pancreatitis in the rat
    H 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...
  22. ncbi request reprint Long-term alcohol exposure changes sensitivity of rat Kupffer cells to lipopolysaccharide
    N 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...
  23. ncbi request reprint Dietary glycine blunts lung inflammatory cell influx following acute endotoxin
    M 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...
  24. ncbi request reprint Cyclosporin A causes a hypermetabolic state and hypoxia in the liver: prevention by dietary glycine
    Z 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...
  25. ncbi request reprint Autonomic nervous system and gut-derived endotoxin: involvement in activation of Kupffer cells after in situ organ manipulation
    P 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...
  26. ncbi request reprint Corn oil rapidly activates nuclear factor-kappaB in hepatic Kupffer cells by oxidant-dependent mechanisms
    I 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...
  27. ncbi request reprint Viral delivery of superoxide dismutase gene reduces cyclosporine A-induced nephrotoxicity
    Z 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...
  28. ncbi request reprint [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...
  29. ncbi request reprint Attenuation of CCl(4)-induced hepatic fibrosis by GdCl(3) treatment or dietary glycine
    C 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...
  30. pmc Dietary glycine prevents peptidoglycan polysaccharide-induced reactive arthritis in the rat: role for glycine-gated chloride channel
    X 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...
  31. ncbi request reprint Viral gene delivery of superoxide dismutase attenuates experimental cholestasis-induced liver fibrosis in the rat
    Z 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...
  32. pmc Evidence that hypoxia markers detect oxygen gradients in liver: pimonidazole and retrograde perfusion of rat liver
    G 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...
  33. ncbi request reprint Comparison of the effect of adenoviral delivery of three superoxide dismutase genes against hepatic ischemia-reperfusion injury
    M 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...
  34. ncbi request reprint Gadolinium chloride-induced hepatocyte proliferation is prevented by antibodies to tumor necrosis factor alpha
    M L Rose
    Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, 27599, USA
    Toxicol Appl Pharmacol 170:39-45. 2001
    ....
  35. ncbi request reprint Reperfusion injury is dramatically increased by gentle liver manipulation during harvest
    P 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...
  36. ncbi request reprint Potent peroxisome proliferators inhibit beta-oxidation in the isolated perfused rat liver
    H 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...
  37. ncbi request reprint Ischemic preconditioning of rat livers against cold storage-reperfusion injury: role of nonparenchymal cells and the phenomenon of heterologous preconditioning
    M 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...
  38. ncbi request reprint Essential role of tumor necrosis factor alpha in alcohol-induced liver injury in mice
    M 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...
  39. ncbi request reprint Food restriction and stimulation of monooxygenation of p-nitroanisole in perfused rat liver
    W 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...
  40. ncbi request reprint Oxidants from nicotinamide adenine dinucleotide phosphate oxidase are involved in triggering cell proliferation in the liver due to peroxisome proliferators
    I Rusyn
    Department of Pharmacology, University of North Carolina at Chapel Hill, 27599, USA
    Cancer Res 60:4798-803. 2000
    ....
  41. ncbi request reprint Novel role of oxidants in the molecular mechanism of action of peroxisome proliferators
    I Rusyn
    Department of Pharmacology and Curriculum in Toxicology, University of North Carolina, Chapel Hill 27599 7365, USA
    Antioxid Redox Signal 2:607-21. 2000
    ....
  42. ncbi request reprint Endothelial cells contain a glycine-gated chloride channel
    S 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...
  43. ncbi request reprint Gene and antisense delivery in alcoholism research
    Y 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...