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Antioxidant activities and redox regulation of interferon-gamma-induced tryptophan metabolism in human monocytes and macrophages.

Abstract
This article summarises studies supporting the proposal that induction of L-tryptophan (Trp) degradation along the kynurenine pathway in human monocytes and macrophages by interferon-gamma (IFN gamma) represents a novel extracellular antioxidant defence that acts to prevent inadvertent oxidative damage to host tissue during inflammation. The studies show that formation and release of the aminophenolic antioxidant 3-hydroxyanthranilic acid (3-HAA) is responsible for the ability of IFN gamma-primed human macrophages to inhibit the oxidation of low density lipoprotein (LDL); an event implicated as an important event in atherogenesis. 3-HAA efficiently inhibits LDL oxidation by acting as an aqueous oxidant scavenger and a synergist for LDL-associated vitamin E. Indoleamine 2,3-dioxygenase activity (IDO) is the initial and rate limiting enzyme of Trp degradation along the kynurenine pathway. Nitric oxide inhibits IDO activity in IFN gamma-primed human macrophages and this may represent a physiological regulatory mechanism of the dioxygenase during inflammation.
AuthorsS R Thomas, R Stocker
JournalAdvances in experimental medicine and biology (Adv Exp Med Biol) Vol. 467 Pg. 541-52 ( 1999) ISSN: 0065-2598 [Print] United States
PMID10721098 (Publication Type: Journal Article, Review)
Chemical References
  • Antioxidants
  • Lipoproteins, LDL
  • oxidized low density lipoprotein
  • Vitamin E
  • 3-Hydroxyanthranilic Acid
  • Interferon-gamma
  • Tryptophan
Topics
  • 3-Hydroxyanthranilic Acid (metabolism, pharmacology)
  • Antioxidants (metabolism, pharmacology)
  • Drug Synergism
  • Humans
  • Interferon-gamma (pharmacology)
  • Lipoproteins, LDL (metabolism)
  • Macrophages (drug effects, immunology, metabolism)
  • Monocytes (drug effects, immunology, metabolism)
  • Oxidation-Reduction
  • Tryptophan (metabolism)
  • Vitamin E (pharmacology)

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