期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 51, 期 9, 页码 1815-1822出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2011.08.008
关键词
Myeloperoxidase; Thiol oxidation; Protein oxidation; Thiocyanate; Smoking; Hypothiocyanous acid; Hypochlorous acid; Free radicals
资金
- Australian Research Council [CE0561607, DP0988311]
- National Health and Medical Research Council [1570829]
- National Heart Foundation [G09S4313, G08S3769, CR08S3959]
Smokers have an elevated risk of atherosclerosis but the origins of this elevated risk are incompletely defined, though evidence supports an accumulation of the oxidant-generating enzyme myeloperoxidase (MPO) in the inflamed artery wall. We hypothesized that smokers would have a high level of thiocyanate (SCN-), a preferred substrate for MPO, which in turn would predispose to thiol oxidation, an established independent risk factor for atherosclerosis. In this study it is shown that on exposure to MPO/H2O2, thiols on plasma proteins from nonsmokers were increasingly oxidized with increasing added SCN- concentrations. Plasma from smokers contained significantly higher endogenous levels of SCN- than that from nonsmokers (131 +/- 31 vs 40 +/- 24 mu M, P<0.0001). When plasma from smokers and nonsmokers was exposed to MPO/H2O2-stimulated oxidation, a strong positive correlation (r = 0.8139, P<0.0001) between the extent of thiol oxidation and the plasma SCN- concentrations was observed. Computational calculations indicate a changeover from HOCl to HOSCN as the major MPO-generated oxidant in plasma, with increasing SCN- levels. These data indicate that plasma SCN- levels are a key determinant of the extent of thiol oxidation on plasma proteins induced by MPO, and implicate HOSCN as an important mediator of inflammation-induced oxidative damage to proteins in smokers. (C) 2011 Elsevier Inc. All rights reserved.
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