Smoking, COPD, and 3-nitrotyrosine levels of plasma proteins.
Smoking, COPD, and 3-nitrotyrosine levels of plasma proteins.
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DOI：
10.1289/ehp.1103745
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发表时间：
2011-09
影响因子：
10.4
通讯作者：
Zangar RC
中科院分区：
文献类型：
--
作者：
Jin H;Webb-Robertson BJ;Peterson ES;Tan R;Bigelow DJ;Scholand MB;Hoidal JR;Pounds JG;Zangar RC
背景：一氧化氮是内皮功能和血液动力学的生理调节剂。一氧化氮的氧化产物可以形成硝基酪氨酸，这是硝化应激的标志。吸烟减少呼出的一氧化氮，其潜在机制可能在吸烟的心血管毒性中很重要。即便如此，目前还不清楚这种影响是由于一氧化氮产生减少还是一氧化氮氧化降解为活性硝化物质增加。预计这两个过程对硝基酪氨酸水平（硝化应激的标志物）具有相反的影响。目的：在这项研究中，我们评估了吸烟和慢性阻塞性肺疾病（COPD）与特定血浆蛋白的硝基酪氨酸修饰的关系，以深入了解硝基酪氨酸形成的调节过程。方法：开发定制抗体微阵列平台以分析血浆中24种蛋白质上的3-硝基酪氨酸修饰水平。在一项横断面研究中，分析了458名个体的血浆样本。结果如下：吸烟者和既往吸烟者血浆蛋白中的平均硝基酪氨酸水平始终低于从不吸烟者，但与肺功能正常的吸烟者相比，COPD吸烟者血浆蛋白中的平均硝基酪氨酸水平升高。结论：吸烟与血浆蛋白中3-硝基酪氨酸水平的广泛降低有关，这与香烟烟雾对内皮一氧化氮产生的抑制作用一致。相反，我们观察到COPD吸烟者的硝基酪氨酸水平高于非COPD吸烟者。这一发现与炎症过程相关的硝化作用增加一致。这项研究提供了一个机制，通过吸烟可以诱导内皮功能障碍，增加心血管疾病的风险。
Background: Nitric oxide is a physiological regulator of endothelial function and hemodynamics. Oxidized products of nitric oxide can form nitrotyrosine, which is a marker of nitrative stress. Cigarette smoking decreases exhaled nitric oxide, and the underlying mechanism may be important in the cardiovascular toxicity of smoking. Even so, it is unclear if this effect results from decreased nitric oxide production or increased oxidative degradation of nitric oxide to reactive nitrating species. These two processes would be expected to have opposite effects on nitrotyrosine levels, a marker of nitrative stress. Objective: In this study, we evaluated associations of cigarette smoking and chronic obstructive pulmonary disease (COPD) with nitrotyrosine modifications of specific plasma proteins to gain insight into the processes regulating nitrotyrosine formation. Methods: A custom antibody microarray platform was developed to analyze the levels of 3-nitrotyrosine modifications on 24 proteins in plasma. In a cross-sectional study, plasma samples from 458 individuals were analyzed. Results: Average nitrotyrosine levels in plasma proteins were consistently lower in smokers and former smokers than in never smokers but increased in smokers with COPD compared with smokers who had normal lung-function tests. Conclusions: Smoking is associated with a broad decrease in 3-nitrotyrosine levels of plasma proteins, consistent with an inhibitory effect of cigarette smoke on endothelial nitric oxide production. In contrast, we observed higher nitrotyrosine levels in smokers with COPD than in smokers without COPD. This finding is consistent with increased nitration associated with inflammatory processes. This study provides insight into a mechanism through which smoking could induce endothelial dysfunction and increase the risk of cardiovascular disease.
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影响因子：
6.6
作者：
Edirisinghe, Indika;Arunachalam, Gnanapragasam;Rahman, Irfan
通讯作者：
Rahman, Irfan
影响因子：
12.3
作者：
Beane J;Sebastiani P;Liu G;Brody JS;Lenburg ME;Spira A
通讯作者：
Spira A
DOI：
10.1073/pnas.88.11.4651
发表时间：
1991-06-01
影响因子：
11.1
作者：
KUBES, P;SUZUKI, M;GRANGER, DN
通讯作者：
GRANGER, DN
DOI：
10.1152/ajpheart.00930.2008
发表时间：
2009-06-01
影响因子：
4.8
作者：
Peluffo, Gonzalo;Calcerrada, Pablo;Radi, Rafael
通讯作者：
Radi, Rafael
影响因子：
4.3
作者：
OHSHIMA, H;FRIESEN, M;BARTSCH, H
通讯作者：
BARTSCH, H