Passive cigarette smoking increases isoprostane formation

被引:28
作者
Ahmadzadehfar, H
Oguogho, A
Efthimiou, Y
Kritz, H
Sinzinger, H
机构
[1] Inst Diagnosis & Treatment Atherosclerosis & Lipi, A-1090 Vienna, Austria
[2] Wilhelm Auerswald Atherosclerosis Res Grp, Vienna, Austria
[3] Austrian Greek Atherosclerosis Prevent Inst, Vienna, Austria
关键词
passive cigarette smoking; isoprostanes; 8-epi-prostaglandin F-2 alpha; oxidation injury; thromboxane; vascular risk;
D O I
10.1016/j.lfs.2005.05.099
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Passive smoking has been demonstrated to exert a variety of deleterious effects eventually resulting in vascular damage. Isoprostanes, a reliable marker of in vivo oxidation injury, have been shown to increase in active cigarette smoking. Data for passive smoking are lacking. We were examining the isoprostane 8-epi-PGF(2 alpha) in 12 smokers and non-smokers exposed daily to passive cigarette smoke for 12 days. Plasma samples stored at liquid nitrogen from people having been examined earlier were used. Prevalues of 8-epi-PGF(2 alpha) are higher in cigarette smokers. Exposure to passive smoking causes a significant increase in 8-epi-PGF(2 alpha) in non-smokers, while in smokers there is only a trendwise increase. After repeated passive smoke exposure, 8-epi-PGF(2 alpha) in non-smokers approaches the respective values of smokers. There is a significant correlation of 8-epi-PGF(2 alpha) to the thromboxane (plasma, serum, conversion from exogenous precursor, 11-dehydro-TYB2) parameters (MDA, HHT- conversion) examined in these patients before. The findings document a significant temporary increase in in vivo oxidation injury due to passive smoke favouring development and/or progression of vascular disease. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:894 / 897
页数:4
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