Hyperoxia and self- or neutrophil-generated O2 metabolites inactivate xanthine oxidase

L. S. Terada, C. J. Beehler, A. Banerjee, J. M. Brown, M. A. Grosso, A. H. Harken, J. M. McCord, J. E. Repine

Research output: Contribution to journalArticlepeer-review

48 Scopus citations

Abstract

Xanthine oxidase (XO) and xanthine dehydrogenase (XD) activities decreased in lungs isolated from rats and cultured lung endothelial cells that had been exposed to hyperoxia. Purified XO activity also decreased after addition of a variety of chemically generated O2 metabolite species (superoxide anion, hydrogen peroxide, hydroxyl radical, or hypochlorous acid), hypoxanthine, or stimulated neutrophils in vitro. XO inactivation by chemically, self-, or neutrophil-generated O2 metabolites was decreased by simultaneous addition of various O2 metabolite scavengers but not their inactive analogues. Since XO appears to contribute to a variety of biological processes and diseases, hyperoxia- or O2 metabolite-mediated decreases in XO activity may be an important cellular control mechanism.

Original languageEnglish (US)
Pages (from-to)2349-2353
Number of pages5
JournalJournal of applied physiology
Volume65
Issue number5
DOIs
StatePublished - 1988

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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