Casella Marta, Miniati Massimo, Monti Simonetta, Minichilli Fabrizio, Bianchi Fabrizio, Simi Silvana
Cell Biology and Cytogenetics Unit, Institute of Clinical Physiology, National Research Council, Pisa, Italy.
Mutagenesis. 2006 Mar;21(2):167-71. doi: 10.1093/mutage/gel015. Epub 2006 Mar 27.
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality in industrialized countries. It is characterized by a progressive airflow limitation resulting from an abnormal inflammatory response of the lungs to inhaled gases and particles. Since oxidative stress is thought to play a role in COPD, and since increased oxidative stress is associated with chromosomal instability in several diseases, we investigated whether such relationship also exists in COPD. Whole blood lymphocytes from 49 COPD patients and 48 age- and sex-matched controls were cultivated in vitro and cytogenetic damage was evaluated by micronucleus (MN) and sister-chromatid-exchange (SCE) assays. In patients with COPD, MN frequency was not significantly different from that of controls. Similarly, SCE frequency did not differ in the two groups suggesting no disturbance in DNA replication. Unlike other diseases characterized by oxidative stress, COPD does not appear to be associated with DNA damage.
慢性阻塞性肺疾病（COPD）是工业化国家发病和死亡的主要原因。其特征是肺部对吸入气体和颗粒的异常炎症反应导致气流进行性受限。由于氧化应激被认为在COPD中起作用，并且由于氧化应激增加与多种疾病中的染色体不稳定有关，我们研究了这种关系在COPD中是否也存在。对49例COPD患者和48例年龄及性别匹配的对照者的全血淋巴细胞进行体外培养，并通过微核（MN）和姐妹染色单体交换（SCE）试验评估细胞遗传损伤。COPD患者的MN频率与对照组无显著差异。同样，两组的SCE频率也无差异，表明DNA复制无干扰。与其他以氧化应激为特征的疾病不同，COPD似乎与DNA损伤无关。
