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Cited by 7,029Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.

Apparent hydroxyl radical production by peroxynitrite: Implications for endothelial injury from nitric oxide and superoxide

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Beckman, J S, Beckman, T W, Chen, J, Marshall, P A, Freeman, B A·1990·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.87.4.1620PMC PMC53527
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Abstract

Superoxide dismutase reduces injury in many disease processes, implicating superoxide anion radical (O2-.) as a toxic species in vivo. A critical target of superoxide may be nitric oxide (NO.) produced by endothelium, macrophages, neutrophils, and brain synaptosomes. Superoxide and NO. are known to rapidly react to form the stable peroxynitrite anion (ONOO-). We have shown that peroxynitrite has a pKa of 7.49 +/- 0.06 at 37 degrees C and rapidly decomposes once protonated with a half-life of 1.9 sec at pH 7.4. Peroxynitrite decomposition generates a strong oxidant with reactivity similar to hydroxyl radical, as assessed by the oxidation of deoxyribose or dimethyl sulfoxide. Product yields indicative of hydroxyl radical were 5.1 +/- 0.1% and 24.3 +/- 1.0%, respectively, of added peroxynitrite. Product formation was not affected by the metal chelator diethyltriaminepentaacetic acid, suggesting that iron was not required to catalyze oxidation. In contrast, desferrioxamine was a potent, competitive inhibitor of peroxynitrite-initiated oxidation because of a direct reaction between desferrioxamine and peroxynitrite rather than by iron chelation. We propose that superoxide dismutase may protect vascular tissue stimulated to produce superoxide and NO. under pathological conditions by preventing the formation of peroxynitrite.

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Crossref · 10.1073/pnas.87.4.1620

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Metadata

Authors
Beckman, J. S., Beckman, T. W., Chen, J., Marshall, P. A., & Freeman, B. A.
Affiliations
  • University of Alabama at Birmingham (US)
  • Department of Anesthesiology, University of Alabama, Birmingham 35233.
ORCID
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1990-02
Volume
87
Issue
4
Pages
1620-1624
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.87.4.1620
PMC
PMC53527
OpenAlex
W2058137293
Cited by
7,029
References
25
Citations by year
2026: 33 · 2025: 43 · 2024: 76 · 2023: 75 · 2022: 84 · 2021: 83 · 2020: 96 · 2019: 94 · 2018: 104 · 2017: 123 · 2016: 123 · 2015: 124 · 2014: 179 · 2013: 160 · 2012: 187
FWCI
67.23
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Heart Association
  • National Institutes of Health (5r01ns024275-04)
  • National Institute of Neurological Disorders and Stroke (NS 24338, NS24275)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
peroxynitrite, hydroxyl radicals, superoxide dismutase, nitric oxide, superoxide, endothelial injury, peroxynitrite decomposition, deferoxamine, deoxyribose oxidation, dimethyl sulfoxide oxidation, pKa, oxidative stress
MeSH terms
Animals, Endothelium, Vascular, Free Radicals, Half-Life, Hydrogen-Ion Concentration, Hydroxides, Kinetics, Models, Biological, Nitrates, Nitric Oxide, Peroxides, Superoxides, Superoxide Dismutase, Hydroxyl Radical

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