DNA damage in peripheral blood of patients with chronic obstructive pulmonary disease (COPD)
DNA damage in peripheral blood of patients with chronic obstructive pulmonary disease (COPD)
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DOI：
10.1016/j.mrgentox.2006.10.002
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发表时间：
2007-01-10
影响因子：
1.9
通讯作者：
Zimermann Teixeira, Paulo Jose
中科院分区：
文献类型：
--
作者：
Maluf, Sharbel Weidner;Mergener, Michelle;Zimermann Teixeira, Paulo Jose
慢性阻塞性肺疾病(COPD)是一种以慢性呼吸道炎症和重塑、肺实质炎症和破坏为特征的疾病，导致呼气性气流阻塞、肺过度充气并失去弹性后坐，以及气体交换障碍。慢性阻塞性肺疾病患者的骨骼肌在休息时会产生自由基，收缩活动时产生的自由基会增加。自由基的过量产生可能会导致氧化剂-抗氧化剂的失衡，有利于氧化剂。本研究采用胞质分裂阻断微核(CBMN)和彗星试验评价COPD患者外周血中的遗传损伤水平。这项研究是对25名COPD患者和25名年龄和性别匹配的对照组进行的。彗星和CBMN检测结果均显示DNA损伤水平增加。慢性阻塞性肺疾病组双核细胞微核率平均为6.72+/-3.02，对照组为4.20+/-2.08(P=0.00233)。COPD组彗星平均值为26.84±19.61，对照组为7.25+/-7.57(P=0.00004)。COPD患者微核率的增加主要归因于断裂事件和DNA扩增，因为核质桥和花蕾的频率也增加了。肺细胞中的氧化应激是破坏肺和循环细胞遗传物质的自由基的持续来源。(C)2006爱思唯尔B.V.保留所有权利。
Chronic obstructive pulmonary disease (COPD) is a condition characterized by chronic airway inflammation and remodeling, lung parenchymal inflammation, and destruction resulting in expiratory airflow obstruction, hyperinflation of the lung with loss of elastic recoil, and impairment of gas exchange. Skeletal muscles in individuals with COPD generate free radicals at rest, and production increases during contractile activity. Overproduction of free radicals may result in oxidant-antioxidant imbalance in favor of oxidants. This study evaluated the levels of genetic damage in peripheral blood of patients with COPD using the cytokinesis-blocked micronucleus (CBMN) and the comet assays. The study was conducted with 25 patients with COPD and 25 controls matched for age and sex. Results of both comet and CBMN assays showed an increase in the level of DNA damage. In the group of patients with COPD, the mean frequency of binucleate cells with micronuclei was 6.72 +/- 3.02, and in the control group, 4.20 +/- 2.08 (p = 0.00233). Mean comet value was 26.84 +/- 19.61 in patients with COPD and 7.25 +/- 7.57 in the control group (p = 0.00004). The increased frequency of micronuclei in patients with COPD was primarily assigned to clastogenic events and DNA amplification because the frequency of nucleoplasmic bridges and buds was also increased. Oxidative stress in lung cells is a constant source of free radicals that damage genetic material of both lung and circulating cells. (c) 2006 Elsevier B.V. All rights reserved.