|
吸烟与肺组织DNA加合物形成关系的研究 |
|
吕京1 杨柯1 崔涛1 谢汇江2 张海青2 孟庆海2 赵志文2 贺锡雯1
【摘要】 目的 探讨吸烟与人肺组织DNA加合物含量的关系以及在肺癌患者与非肺癌患者之间、男女性之间有无差别。方法 提取同期住院原发肺癌患者与非肺癌患者(男各19例, 女各18例)手术切除正常肺组织DNA, 采用32P后标记方法测定DNA加合物含量。结果 吸烟可明显地引起肺组织DNA加合物含量增高。如果控制吸烟因素, 男女之间, 非肺癌患者与肺癌患者之间的肺组织DNA加合物水平差异无统计学意义。结论 人体中DNA加合物水平与生物学效应之间的关系尚需积累更多的资料加以阐明。 【关键词】 肺肿瘤 DNA加合物 吸烟 同位素标记
Studies on the Relationship between Smoking and Formation of DNA Adducts in Lung Tissues L Jing, Yang Ke, Cui Tao, et al. Institute of Occupational Medicine Chinese Academy of Preventive Medicine, Beijing 100050 【Abstract】 Objective To explore the relationship between smoking and contents of DNA adducts in the lung tissues, and to study if there is any its difference between the patients with and without lung cancer and between males and females. Methods DNA was extracted from the normal lung tissues dissected from the concurrently hospitalized patients with and without lung cancer (19 and 18 each for males and females). Contents of DNA adducts in the lung tissues were determined by 32P-postlabelling assay. Results Smoking could cause increase in levels of DNA adducts in the lung tissues. There were no significant difference in DNA adduct levels between the lung tissues from men and women and from the patients with and without lung cancer, after the adjustment for smoking factor. Conclusion More data should be accumulated to elucidate the relationship between DNA adduct levels in the human bodies and its biological effects. 【Key words】 Tumor, lung DNA adduct Smoking Isotope labelling
吸烟可致肺癌的观点已广泛被世人所接受。这主要基于以下研究: ①大量的人群流行病学研究; ②从香烟及其燃烧产物中分离鉴定出大量致突物和致癌物; ③动物实验结果。但人们从没有放弃寻找吸烟与肺癌关系的更直接证据。随着对致癌机理研究的不断深入, 人们发现, 外来化学物进入体内经生物转化生成亲电活性产物, 然后与DNA链上的特异位点结合, 形成共价DNA加合物, 可能是化学物致癌的途径之一。80年代发展起来的DNA加合物测定方法, 特别是32P后标记方法, 由于可用于人体样本的检测, 极大地推动了这一领域内的研究。靶器官内DNA加合物的水平反映的是更直接的外来物对DNA的作用, 尽管人体组织样本十分难得, 还是引起了人们极大的关注。通过对17例肺癌患者肺组织DNA加合物含量分析, Phillips等[1]于1988年在《Nature》 杂志上提出吸烟可导致肺组织DNA加合物水平升高。国内学者分析了3[1] [2] 下一页 上一个医学论文: 工频磁场抑制细胞缝隙连接通讯功能的剂量 下一个医学论文: 接触二硫化碳人群肾上腺皮质功能监测研究
|
|
|
|
|
|
|