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    Heme oxygenase-1 induction in hepatocytes and non-parenchymal cells protects against liver injury during endotoxemia

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    Author
    Dorman, Robert
    Bajt, Mary
    Farhood, Anwar
    Mayes, January
    Jaeschke, Hartmut
    Affiliation
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Liver Research Institute, University of Arizona, 1501 N. Campbell Avenue, Tucson, Arizona 85724, USA
    Department of Pathology, University of Texas Health Science Center, Houston, Texas 77030, USA
    Issue Date
    2004
    
    Metadata
    Show full item record
    Publisher
    BioMed Central
    Citation
    Comparative Hepatology 2004, 3(Suppl 1):S42 http://www.comparative-hepatology.com/content/3/S1/S42
    Journal
    Comparative Hepatology
    Rights
    © Dorman et al; licensee BioMed Central Ltd 2004.
    Collection Information
    This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
    Abstract
    INTRODUCTION:Heme oxygenase-1 (HO-1) is a stress response enzyme, which catalyses the breakdown of heme into biliverdin-IX alpha, carbon monoxide and ferrous iron. Under situations of oxidative stress, heat stress, ischemia/reperfusion injury or endotoxemia, HO-1 has been shown to be induced and to elicit a protective effect. The mechanism of how this protective effect is executed is unknown.RESULTS:HO-1 induction with cobalt protoporphorin (Co-PP) dose-dependently protected against apoptotic cell death as well as neutrophil-mediated oncosis in the galactosamine/endotoxin (Gal/ET) shock model. Induction of HO-1 with Co-PP dose-dependently protected against neutrophil-mediated oncosis as indicated by attenuated ALT release and TNF-mediated apoptotic cell death as indicated by reduced caspase-3 activation. HO-1 induction did not attenuate Gal/ET-induced TNF-alpha formation. Furthermore, a similar protective effect with the high dose of Co-PP was observed when animals were treated with Gal/TNF-alpha.CONCLUSIONS:HO-1 induction attenuates apoptosis and neutrophil-mediated oncosis in the Gal/ET shock model. However, the protective effect is not due to the reduction of TNF-alpha release or the attenuation of neutrophil accumulation in the liver sinusoids.
    EISSN
    1476-5926
    DOI
    10.1186/1476-5926-2-S1-S42
    Version
    Final published version
    Additional Links
    http://www.comparative-hepatology.com/content/3/S1/S42
    ae974a485f413a2113503eed53cd6c53
    10.1186/1476-5926-2-S1-S42
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    UA Faculty Publications

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