Cited by 686Neutrophil, Myeloperoxidase and Oxidative MechanismsNitric Oxide and Endothelin EffectsRedox biology and oxidative stress

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Nitric oxide, an endothelial cell relaxation factor, inhibits neutrophil superoxide anion production via a direct action on the NADPH oxidase.

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Clancy, R M, Leszczynska-Piziak, J, Abramson, S B·1992·Journal of Clinical Investigation

DOI 10.1172/jci115929PMC PMC329973

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Abstract

Nitric oxide provokes vasodilation and inhibits platelet aggregation. We examined the effect of nitric oxide on superoxide anion production by three sources: activated intact neutrophils, xanthine oxidase/hypoxanthine, and the NADPH oxidase. Nitric oxide significantly inhibited the generation of superoxide anion by neutrophils exposed to either FMLP (10(-7)M) or PMA (150 ng/ml) (IC50 = 30 microM). To determine whether the effect of nitric oxide on the respiratory burst was due to simple scavenging of O2+, kinetic studies that compared effects on neutrophils and the cell-free xanthine oxidase system were performed. Nitric oxide inhibited O2+ produced by xanthine oxidase only when added simultaneously with substrate, consistent with the short half-life of NO in oxygenated solution. In contrast, the addition of nitric oxide to neutrophils 20 min before FMLP resulted in the inhibition of O2+ production, which suggests formation of a stable intermediate. The effect of nitric oxide on the cell-free NADPH oxidase superoxide-generating system was also examined: The addition of NO before arachidonate activation (t = -6 min) significantly inhibited superoxide anion production. Nitric oxide did not inhibit O2+ when added at NADPH initiation (t = 0). Treatment of the membrane but not cytosolic component of the oxidase was sufficient to inhibit O2+ generation. The data suggest that nitric oxide inhibits neutrophil O2+ production via direct effects on membrane components of the NADPH oxidase. This action must occur before the assembly of the activated complex.

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Authors: Clancy, R. M., Leszczynska-Piziak, J., & Abramson, S. B.
Affiliations: NYU Langone Health (US)
ORCID: Clancy, R M
Abramson, S B
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1992-09-01
Volume: 90
Issue: 3
Pages: 1116-1121
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci115929
PMC: PMC329973
OpenAlex: W2139533485
Cited by: 686
References: 54
Citations by year: 2026: 1 · 2025: 5 · 2024: 5 · 2023: 6 · 2022: 1 · 2021: 3 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 9 · 2016: 6 · 2015: 11 · 2014: 10 · 2013: 5 · 2012: 9
FWCI: 13.70
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: nitric oxide, neutrophils, superoxide production, NADPH oxidase, respiratory burst, fMLP, PMA, arachidonic acid, oxygen radical scavenging
MeSH terms: Calcium, Cells, Cultured, Humans, NADH, NADPH Oxidoreductases, Neutrophils, Nitric Oxide, Superoxides, Xanthine Oxidase, Cell Degranulation, NADPH Oxidases

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Nitric oxide, an endothelial cell relaxation factor, inhibits neutrophil superoxide anion production via a direct action on the NADPH oxidase.

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