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Research ArticleArticle

Peroxisomes Are Involved in the Swift Increase in Alcohol Metabolism

Blair U. Bradford, Nobuyuki Enomoto, Kenichi Ikejima, Michelle L. Rose, Heidi K. Bojes, Donald T. Forman and Ronald G. Thurman
Journal of Pharmacology and Experimental Therapeutics January 1999, 288 (1) 254-259;
Blair U. Bradford
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Nobuyuki Enomoto
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Kenichi Ikejima
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Michelle L. Rose
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Heidi K. Bojes
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Donald T. Forman
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Ronald G. Thurman
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Abstract

The purpose of this study was to determine whether catalase-dependent alcohol metabolism is activated by alcohol (i.e., swift increase in alcohol metabolism). When ethanol or the selective substrate for catalase, methanol, was given (5.0 g/kg) in vivo 2 to 3 h before liver perfusion, methanol and oxygen metabolism were increased significantly. This increase was blocked when the specific Kupffer cell toxicant GdCl3 was administered 24 h before perfusion. These data support the hypothesis that catalase-dependent alcohol metabolism is activated by acute alcohol and that Kupffer cells are involved. Ethanol treatment in vivo increased ketogenesis from endogenous fatty acids nearly 3-fold and increased plasma triglycerides and hepatic acyl CoA synthetase activity; all increases were blocked by GdCl3. These findings support the hypothesis that ethanol increases H2O2 supply for catalase-dependent alcohol metabolism by increasing fatty acid supply. Infusion of oleate stimulated oxygen uptake 1.5-fold and methanol metabolism 4-fold, but these parameters were not altered by GdCl3. Moreover, the effects of ethanol treatment were blocked by the cyclooxygenase inhibitor indomethacin, and prostaglandin E2(PGE2) was increased more than 200% in media from cultured Kupffer cells from rats treated with ethanol in vivo. Furthermore, lipoprotein lipase activity in retroperitoneal fat pads, which is known to be inhibited by PGE2, was reduced 70% by ethanol. These data are consistent with the hypothesis that Kupffer cells play a key role in activation of catalase-dependent alcohol metabolism, most likely by producing mediators (e.g., PGE2) that inhibit lipoprotein lipase, increase the supply of fatty acids to the liver, and increase generation of H2O2 via peroxisomal β-oxidation.

Footnotes

  • Send reprint requests to: Dr. Ronald G. Thurman, Doctor of Philosophy, Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, CB #7365 Mary Ellen Jones Building, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7365. E-mail:thurman{at}med.unc.edu.

  • ↵1 This work was supported in part by grants from NIAAA and the Center for Gastrointestinal Biology and Disease.

  • Abbreviations:
    PGE2
    prostaglandin E2
    LPL
    lipoprotein lipase
    ADH
    alcohol dehydrogenase
    ANOVA
    analysis of variance
    SIAM
    swift increase in alcohol metabolism
    • Received June 25, 1998.
    • Accepted August 26, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 1
1 Jan 1999
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Research ArticleArticle

Peroxisomes Are Involved in the Swift Increase in Alcohol Metabolism

Blair U. Bradford, Nobuyuki Enomoto, Kenichi Ikejima, Michelle L. Rose, Heidi K. Bojes, Donald T. Forman and Ronald G. Thurman
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 254-259;

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Research ArticleArticle

Peroxisomes Are Involved in the Swift Increase in Alcohol Metabolism

Blair U. Bradford, Nobuyuki Enomoto, Kenichi Ikejima, Michelle L. Rose, Heidi K. Bojes, Donald T. Forman and Ronald G. Thurman
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 254-259;
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