Smoking cessation reverses DNA double-strand breaks in human mononuclear cells.
Smoking cessation reverses DNA double-strand breaks in human mononuclear cells.
复制标题
戒烟会逆转人类单核细胞中的DNA双链断裂。
DOI：
10.1371/journal.pone.0103993
复制
发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Yoshizumi M
中科院分区：
文献类型：
--
作者：
Ishida M;Ishida T;Tashiro S;Uchida H;Sakai C;Hironobe N;Miura K;Hashimoto Y;Arihiro K;Chayama K;Kihara Y;Yoshizumi M
吸烟是动脉粥样硬化性心血管疾病的主要危险因素，这是造成很大一部分吸烟相关死亡的原因。然而，吸烟诱发这种病理的确切机制尚未完全阐明。基于对动脉粥样硬化病变中最有害的DNA损伤类型DNA双链断裂（DSBs）的观察，我们假设吸烟与DSBs之间存在直接关联。本研究的目的是通过检测外周单核细胞（MNCs），探讨吸烟是否会诱发dsb，而戒烟是否会逆转体内dsb。DNA和DSBs氧化修饰的免疫反应性在人动脉粥样硬化病变中增加，而在邻近正常区域则没有增加。利用抗组蛋白H2AX磷酸化形式（γ-H2AX）的抗体，可以检测从志愿者血液中分离的人MNCs中的DSBs为细胞学上可见的“病灶”。年轻健康的积极吸烟者（n = 15）与非吸烟者（n = 12）相比，γ-H2AX灶数增加（灶数/细胞：中位数，0.37/细胞；四分位数间距[IQR]， 0.31-0.58比4.36/细胞；IQR, 3.09-7.39, p<0.0001）。戒烟1个月降低γ-H2AX灶数（中位数为4.44/细胞；IQR为4.36 ~ 5.24 ~ 0.28/细胞；IQR为0.12 ~ 0.53,p<0.05）。γ-H2AX焦点数与呼出一氧化碳水平呈正相关（r = 0.75, p<0.01）。吸烟在体内诱导人类跨国公司的dsb，重要的是，戒烟1个月导致dsb下降到与非吸烟者相当的水平。这些数据强化了吸烟引起dsb的观念，并强调了戒烟的重要性。
Cigarette smoking is a major risk factor for atherosclerotic cardiovascular disease, which is responsible for a significant proportion of smoking-related deaths. However, the precise mechanism whereby smoking induces this pathology has not been fully delineated. Based on observation of DNA double-strand breaks (DSBs), the most harmful type of DNA damage, in atherosclerotic lesions, we hypothesized that there is a direct association between smoking and DSBs. The goal of this study was to investigate whether smoking induces DSBs and smoking cessation reverses DSBs in vivo through examination of peripheral mononuclear cells (MNCs). Immunoreactivity of oxidative modification of DNA and DSBs were increased in human atherosclerotic lesions but not in the adjacent normal area. DSBs in human MNCs isolated from the blood of volunteers can be detected as cytologically visible “foci” using an antibody against the phosphorylated form of the histone H2AX (γ-H2AX). Young healthy active smokers (n = 15) showed increased γ-H2AX foci number when compared with non-smokers (n = 12) (foci number/cell: median, 0.37/cell; interquartile range [IQR], 0.31–0.58 vs. 4.36/cell; IQR, 3.09–7.39, p<0.0001). Smoking cessation for 1 month reduced the γ-H2AX foci number (median, 4.44/cell; IQR, 4.36–5.24 to 0.28/cell; IQR, 0.12–0.53, p<0.05). A positive correlation was noted between γ-H2AX foci number and exhaled carbon monoxide levels (r = 0.75, p<0.01). Smoking induces DSBs in human MNCs in vivo, and importantly, smoking cessation for 1 month resulted in a decrease in DSBs to a level comparable to that seen in non-smokers. These data reinforce the notion that the cigarette smoking induces DSBs and highlight the importance of smoking cessation.
登录
查看更多内容
影响因子：
158.5
作者：
Darby, Sarah C.;Ewertz, Marianne;Hall, Per
通讯作者：
Hall, Per
DOI：
10.1016/j.mrgentox.2009.06.009
发表时间：
2009-08
影响因子：
1.9
作者：
Albino, Anthony P.;Jorgensen, Ellen D.;Rainey, Patrick;Gillman, Gene;Clark, T. Jeffrey;Gietl, Diana;Zhao, Hong;Traganos, Frank;Darzynkiewicz, Zbigniew
通讯作者：
Darzynkiewicz, Zbigniew
影响因子：
37.8
作者：
Kunieda, Takeshige;Minamino, Tohru;Komuro, Issei
通讯作者：
Komuro, Issei
影响因子：
--
作者：
Rahman, Amirah Abdul;Karim, Norwahidah Abdul;Ngah, Wan Zurinah Wan
通讯作者：
Ngah, Wan Zurinah Wan
影响因子：
21.3
作者：
Rodier, Francis;Coppe, Jean-Philippe;Patil, Christopher K.;Hoeijmakers, Wieteke A. M.;Munoz, Denise P.;Raza, Saba R.;Freund, Adam;Campeau, Eric;Davalos, Albert R.;Campisi, Judith
通讯作者：
Campisi, Judith