氡致小鼠肺损伤及对肺上皮细胞凋亡和p53蛋白表达影响  

Radon induced lung injury and pulmonary epithelial cells apoptosis and p53 protein expression in mice

作　　者：朴春南[1] 田梅[1] 刘建香[1] 阮健磊[1] 苏旭[1] 

机构地区：[1]中国疾病预防控制中心辐射防护与核安全医学所,北京100088

出　　处：《中国职业医学》2011年第2期113-116,共4页China Occupational Medicine

基　　金：科技部科研院所社会公益研究专项资助项目(2005DIB1J087)

摘　　要：目的观察氡吸入染毒小鼠肺及支气管组织的病理学改变、肺细胞凋亡及p53蛋白表达的变化。方法建立氡染毒小鼠模型,观察吸入不同剂量即30和60个工作水平月(WLM)和不同时间段(24 h、30 d、90 d和180 d)氡小鼠肺组织的病理变化;采用TUNEL法检测小鼠肺上皮细胞凋亡程度;用W estern-b lot技术测定小鼠肺及支气管组织p53蛋白的表达水平。结果病理学结果显示,染毒后肺组织的病理表现存在多样性和时相性,早期为急性损伤性反应,后期演变为上皮细胞及肺间质成纤维细胞的增生及组织的纤维化;随着染毒剂量的增加和染毒后随着时间的延续,小鼠肺组织中的肺上皮细胞凋亡指数及p53蛋白表达量比对照组明显升高。结论氡吸入染毒可对小鼠肺造成不同类型的病理损伤,p53在氡吸入导致的肺上皮细胞凋亡过程中可能起到了一定的作用。Objective To observe the pathological changes,cell apoptosis and the expression of p53 protein in lung and bronchus of radon-exposed mice.Methods Male BALB/c mice were exposed to radon and its progeny with the cumulative doses of 30 and 60 working level month（WLM） respectively,and then were executed at different time points（24 hours、30、90 or 180 days）.Pulmonary epithelial cells apoptosis was detected by terminal deoxynucleotidy transferase-mediated dUTP-biotin nick end labeling（TUNEL）.The pathological changes of lung and bronchus were analyzed,and the expressed levels of p53 in lung and bronchus were measured by western-blot.Results The pathological changes in lung and bronchus of radon-exposed mice were diversity and dynamic.After radon-exposure,the lung and bronchus experienced 3 stages：early acute inflammation,proliferation and pulmonary fibrosis.The apoptotic index and p53 protein in lung and bronchus were significantly higher than those of the control group with the increase of dose and the time of raising.Conclusion The lung and bronchus were injured after the exposure to radon and its progeny,and p53 may play an important role in the procedure of radon-induced pulmonary epithelial cells apoptosis of the lung injured cells.

关 键 词：氡 肺损伤 病理学 凋亡 P53 

分 类 号：X591[环境科学与工程—环境工程] R135.2[医药卫生—劳动卫生]