Is the endogenous peroxyl-radical scavenging capacity of plasma protective in systemic inflammatory disorders in humans?

Kelvin Tsai, Tai Ger Hsu, Chi Woon Kong, Kuan Chia Lin, L. U. Fung-Jou

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Systemic inflammatory response syndrome (SIRS) in humans is associated with heightened intravascular oxidative stress. The clinical significance of plasma endogenous antioxidative capability in SIRS remains undetermined. Time-sequence changes of plasma total radical-trapping antioxidant parameter (TRAP) and its components were measured in 135 patients with various clinical conditions leading to SIRS. The results were correlated with clinical parameters. Plasma TRAP significantly depressed upon diagnosis of SIRS (SIRS vs. healthy subjects (n = 50), 605.7 ± 20.4 vs. 803.4 ± 30.8 μM Trolox equivalent, p < .001). In survivors (n = 86), TRAP declined further during the course of SIRS, followed by a mild recovery at the end of follow-up. General linear mixed model analysis revealed that uric acid, vitamin C, vitamin E and unidentified antioxidants contributed to most of the changes in TRAP (each factor p < .001). In nonsurvivors (n = 49), TRAP increased steadily until death, and the increase was predominantly the result of the increased contribution of bilirubin (p < .01). Higher TRAP levels were not correlated with diminished blood oxidants formation (r = -0.13, p > .05), lower intensity of lipid peroxidation (r = 0.261, p < .05) or lesser disease severity of SIRS. The results do not support the hypothesis that the endogenous peroxyl radical scavenging ability of plasma plays a protective role in the course of SIRS. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)926-933
Number of pages8
JournalFree Radical Biology and Medicine
Issue number6
Publication statusPublished - Mar 15 2000
Externally publishedYes



  • Acute-phase reactions
  • Antioxidants
  • Chemiluminescence
  • Disease severity
  • Inflammation
  • Oxidative stress
  • Reactive oxygen species
  • Survival

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

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