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Cytoprotective function of nitric oxide: inactivation of superoxide radicals produced by human leukocytes.

Authors
  • Rubanyi, G M
  • Ho, E H
  • Cantor, E H
  • Lumma, W C
  • Botelho, L H
Type
Published Article
Journal
Biochemical and biophysical research communications
Publication Date
Dec 31, 1991
Volume
181
Issue
3
Pages
1392–1397
Identifiers
PMID: 1662497
Source
Medline
License
Unknown

Abstract

The oxygen-derived free radical superoxide anion (.O2-) plays an important role in the pathogenesis of various diseases. Recent demonstrations that .O2- inactivates the potent vasodilator endothelium-derived relaxing factor (EDRF) and that EDRF is probably nitric oxide (NO) suggest that EDRF(NO) may act as an endogenous free radical scavenger. This hypothesis was tested in an in vitro system by analyzing the effect of authentic NO (dilutions of a saturated aqueous solution) on .O2- production (detected spectrophotometrically as reduction of cytochrome c) by fMet-Leu-Phe-activated human leukocytes (PMN). NO depressed the rate of reduction of cytochrome c by .O2- released from PMN's or generated from the oxidation of hypoxanthine by xanthine oxidase. This effect was concentration-dependent and occurred at dilutions of the saturated NO solution (1:250 to 1:10) which inhibited platelet aggregation. NO had no direct effect on cytochrome c or on xanthine oxidase. These observations indicate that NO(EDRF) can be regarded as a scavenger of superoxide anion and they suggest that EDRF(NO) may provide a chemical barrier to cytotoxic free radicals (.O2-).

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