Peroxynitrite-mediated oxidation of dihydrorhodamine 123 occurs in early stages of endotoxic and hemorrhagic shock and ischemia-reperfusion injury

Csaba Szabó, Andrew L. Salzman, Harry Ischiropoulos

    Research output: Contribution to journalArticle

    161 Scopus citations

    Abstract

    To quantify peroxynitrite production during shock, we measured oxidation of dihydrorhodamine 123 in rats. In endotoxic and hemorrhagic shock and splanchic ischemia-reperfusion, dihydrorhodamine oxidation rapidly increased, which was prevented by inhibition of endothelial nitric oxide (·NO) synthase (ecNOS). Thus, peroxynitrite is already formed at early stages of shock from ecNOS-derived ·NO. Overproduction of ·NO by the inducible NOS at late shock was not associated with additional increases in dihydrorhodamine oxidation. ecNOS inhibition enhanced dihydrorhodamine oxidation in control rats. These latter findings may be explained by ·NO-mediated inhibition of peroxynitrite-induced dihydrorhodamine oxidation, a phenomenon also observed in vitro.

    Original languageEnglish (US)
    Pages (from-to)229-232
    Number of pages4
    JournalFEBS Letters
    Volume372
    Issue number2-3
    DOIs
    StatePublished - Sep 25 1995

    Keywords

    • Constitutive
    • Endotoxin
    • Inflammation
    • Nitric oxide
    • Nitric oxide synthase
    • Peroxynitrite
    • Rhodamine
    • Shock
    • Superoxide

    ASJC Scopus subject areas

    • Biophysics
    • Structural Biology
    • Biochemistry
    • Molecular Biology
    • Genetics
    • Cell Biology

    Fingerprint Dive into the research topics of 'Peroxynitrite-mediated oxidation of dihydrorhodamine 123 occurs in early stages of endotoxic and hemorrhagic shock and ischemia-reperfusion injury'. Together they form a unique fingerprint.

  • Cite this