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

Csaba Szabo, Andrew L. Salzman, Harry Ischiropoulos

Research output: Contribution to journalArticle

162 Citations (Scopus)

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
Externally publishedYes

Fingerprint

Peroxynitrous Acid
Hemorrhagic Shock
Septic Shock
Reperfusion Injury
Shock
Nitric Oxide
Oxidation
Nitric Oxide Synthase Type III
Reperfusion
Rat control
Ischemia
Rats
dihydrorhodamine 123

Keywords

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

ASJC Scopus subject areas

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

Cite this

Peroxynitrite-mediated oxidation of dihydrorhodamine 123 occurs in early stages of endotoxic and hemorrhagic shock and ischemia-reperfusion injury. / Szabo, Csaba; Salzman, Andrew L.; Ischiropoulos, Harry.

In: FEBS Letters, Vol. 372, No. 2-3, 25.09.1995, p. 229-232.

Research output: Contribution to journalArticle

@article{6412bff5a63a46959b978efd73126ed4,
title = "Peroxynitrite-mediated oxidation of dihydrorhodamine 123 occurs in early stages of endotoxic and hemorrhagic shock and ischemia-reperfusion injury",
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.",
keywords = "Constitutive, Endotoxin, Inflammation, Nitric oxide, Nitric oxide synthase, Peroxynitrite, Rhodamine, Shock, Superoxide",
author = "Csaba Szabo and Salzman, {Andrew L.} and Harry Ischiropoulos",
year = "1995",
month = "9",
day = "25",
doi = "10.1016/0014-5793(95)00984-H",
language = "English (US)",
volume = "372",
pages = "229--232",
journal = "FEBS Letters",
issn = "0014-5793",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - Peroxynitrite-mediated oxidation of dihydrorhodamine 123 occurs in early stages of endotoxic and hemorrhagic shock and ischemia-reperfusion injury

AU - Szabo, Csaba

AU - Salzman, Andrew L.

AU - Ischiropoulos, Harry

PY - 1995/9/25

Y1 - 1995/9/25

N2 - 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.

AB - 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.

KW - Constitutive

KW - Endotoxin

KW - Inflammation

KW - Nitric oxide

KW - Nitric oxide synthase

KW - Peroxynitrite

KW - Rhodamine

KW - Shock

KW - Superoxide

UR - http://www.scopus.com/inward/record.url?scp=0029148018&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029148018&partnerID=8YFLogxK

U2 - 10.1016/0014-5793(95)00984-H

DO - 10.1016/0014-5793(95)00984-H

M3 - Article

VL - 372

SP - 229

EP - 232

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 2-3

ER -