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

Citation
Kv. Tsai et al., Is the endogenous peroxyl-radical scavenging capacity of plasma protectivein systemic inflammatory disorders in humans?, FREE RAD B, 28(6), 2000, pp. 926-933
Citations number
37
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
08915849 → ACNP
Volume
28
Issue
6
Year of publication
2000
Pages
926 - 933
Database
ISI
SICI code
0891-5849(20000315)28:6<926:ITEPSC>2.0.ZU;2-T
Abstract
Systemic inflammatory response syndrome (SIRS) in humans is associated with heightened intravascular oxidative stress. The clinical significance of pl asma endogenous antioxidative capability in SLRS remains undetermined. Time -sequence changes of plasma total radical-trapping antioxidant parameter (T RAP) and its components were measured in 135 patients with various clinical conditions leading to SIPS. The results were correlated with clinical para meters. Plasma TRAP significantly depressed upon diagnosis of SIPS (SIRS vs , healthy subjects (n = 50), 605.7 +/- 20.4 vs. 803.4 +/- 30.8 mu M 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. Ge neral linear mixed model analysis revealed that uric acid, vitamin C, vitam in E and unidentified antioxidants contributed to most of the changes in TR AP (each factor p < .001). In nonsurvivors (n = 49), TRAP increased steadil y until death, and the increase was predominantly the result of the increas ed contribution of bililrubin (p < .01). Higher TRAP levels were not correl ated with diminished blood oxidants formation (r = -0.13, p > .05), lower i ntensity of lipid peroxidation (r = 0.261, p < .05) or lesser disease sever ity 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. (C) 2000 Elsevier Science Inc.