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Research ArticleArticle

Role of Lipid Peroxidation in Dapsone-Induced Hemolytic Anemia

David C. McMillan, Charles B. Jensen and David J. Jollow
Journal of Pharmacology and Experimental Therapeutics December 1998, 287 (3) 868-876;
David C. McMillan
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Charles B. Jensen
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David J. Jollow
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Abstract

Dapsone hydroxylamine (DDS-NOH) is a direct-acting hemolytic agent responsible for dapsone-induced hemolytic anemia in the rat. The hemolytic activity of DDS-NOH is associated with the formation of disulfide-linked hemoglobin adducts on membrane skeletal proteins. We have postulated that this membrane protein “damage” is a consequence of DDS-NOH-induced oxidative stress within the red cell and that it serves as the trigger for premature removal of injured but intact red cells from the circulation by splenic macrophages. Oxidative stress has also been associated with the induction of lipid peroxidation, and it is possible that direct damage to the lipoidal membrane may play a role in the premature sequestration of the damaged cells in the spleen. To investigate this possibility, rat and human red cells were incubated with hemolytic concentrations of DDS-NOH and examined for evidence of lipid peroxidation using two independent assays: thiobarbituric acid-reactive substances formation andcis-paranaric acid degradation. Phenylhydrazine, which is known to induce lipid peroxidation in red cells, was used as a positive control. The extent of thiobarbituric acid-reactive substances formation and cis-paranaric acid degradation in DDS-NOH-treated rat and human red cells was not significantly different from that in control cells. In contrast, thiobarbituric acid-reactive substances formation and cis-paranaric acid degradation were significantly increased in red cells treated with hemolytic concentrations of the positive control, phenylhydrazine. These data suggest that lipid peroxidation is not involved in the mechanism underlying dapsone-induced hemolytic anemia.

Footnotes

  • Send reprint requests to: David C. McMillan, Ph.D., Dept. of Pharmacology, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425.

  • ↵1 Supported by NIH Grant HL-30038. These studies were presented in part at the 35th Annual Meeting of the Society of Toxicology, March 10 to 14, 1996, Anaheim, CA, and published in abstract form in Fundamental and Applied Toxicology (Suppl.)30:340, 1996.

  • ↵2 Present address: Biochemical Toxicology Dept., GL992, Toxicology Division, Lilly Research Laboratories, Eli Lilly & Co., P.O. Box 708, Greenfield, IN 46140.

  • Abbreviations:
    DDS-NOH
    dapsone hydroxylamine
    cPnA
    cis-paranaric acid
    TBARS
    thiobarbituric acid-reactive substances
    PBSG
    isotonic phosphate-buffered saline with 10 mM glucose
    MDA
    malondialdehyde
    GSH
    reduced glutathione
    DTT
    dithiothreitol
    • Received January 23, 1997.
    • Accepted June 17, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 287, Issue 3
1 Dec 1998
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Research ArticleArticle

Role of Lipid Peroxidation in Dapsone-Induced Hemolytic Anemia

David C. McMillan, Charles B. Jensen and David J. Jollow
Journal of Pharmacology and Experimental Therapeutics December 1, 1998, 287 (3) 868-876;

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Research ArticleArticle

Role of Lipid Peroxidation in Dapsone-Induced Hemolytic Anemia

David C. McMillan, Charles B. Jensen and David J. Jollow
Journal of Pharmacology and Experimental Therapeutics December 1, 1998, 287 (3) 868-876;
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