The involvement of peripheral polymorphonuclear leukocytes in the oxidative stress and inflammation among cigarette smokers.
The involvement of peripheral polymorphonuclear leukocytes in the oxidative stress and inflammation among cigarette smokers.
复制标题
外周多形核白细胞参与吸烟者的氧化应激和炎症。
DOI：
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
B. Kristal
中科院分区：
文献类型：
--
作者：
S. Sela;R. Shurtz;J. Awad;G. Shapiro;Lubna Nasser;S. Shasha;B. Kristal
背景
吸烟是内皮功能障碍和动脉粥样硬化进展的一个众所周知的危险因素。氧化应激和炎症最近被牵连在内皮功能障碍。
目标
评估多形核白细胞对吸烟者全身氧化应激和炎症的共同作用。
方法
研究组包括41名年龄为45.0 +/- 11.5（范围31-67岁）的长期吸烟、其他方面健康的男性和41名年龄为42.6 +/- 11.3（范围31-65岁）的非吸烟男性，作为对照组。通过测量分离的佛波醇12-肉豆蔻酸酯13-乙酸酯刺激的PMNL的超氧化物释放速率和血浆还原型（GSH）和氧化型（GSSG）谷胱甘肽水平来评估氧化应激的潜在产生。通过以下方法间接评估炎症：a）测定PMNL的体外存活率，反映细胞坏死; B）体内外周PMNL计数，反映细胞募集;和c）血浆碱性磷酸酶水平，表明PMNL活化和脱粒。
结果
PMA刺激的PMNL从吸烟者释放超氧化物的速度比PMNL从控制。吸烟者血浆GSH水平降低，GSSG水平升高。在体外培养的控制和吸烟者的血清中的吸烟者的PMNL引起坏死，而控制血清提高吸烟者PMNL的生存。吸烟者的PMNL计数，虽然在正常范围内，显着高于对照组。吸烟者血浆ALP水平显著高于对照组，并与超氧化物释放和PMNL计数呈正相关。
结论
我们的研究表明，吸烟者的PMNL在体内引发，同时促进全身氧化应激和炎症，使吸烟者易患内皮功能障碍，并部分解释了吸烟者中发现的加速动脉粥样硬化。
BACKGROUND
Cigarette smoking is a well-known risk factor for the development of endothelial dysfunction and the progression of atherosclerosis. Oxidative stress and inflammation have recently been implicated in endothelial dysfunction.
OBJECTIVES
To assess the concomitant contribution of polymorphonuclear leukocytes to systemic oxidative stress and inflammation in cigarette smokers.
METHODS
The study group comprised 41 chronic cigarette-smoking, otherwise healthy males aged 45.0 +/- 11.5 (range 31-67 years) and 41 male non-smokers aged 42.6 +/- 11.3 (range 31-65) who served as the control group. The potential generation of oxidative stress was assessed by measuring the rate of superoxide release from separated, phorbol 12-myristate 13-acetate-stimulated PMNL and by plasma levels of reduced (GSH) and oxidized (GSSG) glutathione. Inflammation was estimated indirectly by: a) determining the in vitro survival of PMNL, reflecting cell necrosis; b) in vivo peripheral PMNL counts, reflecting cell recruitment; and c) plasma alkaline phosphatase levels, indicating PMNL activation and degranulation.
RESULTS
PMA-stimulated PMNL from cigarette smokers released superoxide at a faster rate than PMNL from the controls. Smokers had decreased plasma GSH and elevated GSSG levels. In vitro incubation of control and smokers' PMNL in sera of smokers caused necrosis, while control sera improved smoker PMNL survival. Smokers' PMNL counts, although in the normal range, were significantly higher than those of controls. Plasma ALP levels in smokers were significantly higher than in controls and correlated positively with superoxide release and PMNL counts.
CONCLUSIONS
Our study shows that PMNL in smokers are primed in vivo, contribution concomitantly to systemic oxidative stress and inflammation that predispose smokers to endothelial dysfunction, and explains in part the accelerated atherosclerosis found in smokers.
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DOI：
10.1161/01.atv.17.10.2167
发表时间：
1997-10-01
影响因子：
8.7
作者：
Tracy, RP;Psaty, BM;Kuller, LH
通讯作者：
Kuller, LH
DOI：
--
发表时间：
1994-07
期刊：
The Journal of laboratory and clinical medicine
影响因子：
--
作者：
M. Qian;J. Eaton
通讯作者：
M. Qian;J. Eaton
抗坏血酸补充剂对吸烟者低密度脂蛋白氧化的影响。
影响因子：
5.3
作者：
Fuller,CJ;Grundy,SM;Norkus,EP;Jialal,I
通讯作者：
Jialal,I
影响因子：
120.7
作者：
Howard, G;Wagenknecht, LE;Tell, GS
通讯作者：
Tell, GS
影响因子：
8.3
作者：
ALEXANDER, RW
通讯作者：
ALEXANDER, RW