氡染毒诱导小鼠肺组织细胞凋亡的机制研究  

Studies on the Mechanism of Apoptasis by Radon in Lung Tissue of 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辐射流行病室,北京100088

出　　处：《中国辐射卫生》2011年第2期142-143,145,共3页Chinese Journal of Radiological Health

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

摘　　要：目的研究氡诱发小鼠肺细胞凋亡的机制。方法建立氡染毒小鼠模型,将小鼠分为氡吸入染毒不同剂量组(0.02、30和60WLM)和不同时间段组(24h、30d和90d);采用TUNEL法检测小鼠肺组织细胞凋亡程度;采用免疫组化法,检测各组肺组织p53蛋白及Bcl-2/Bax表达情况。结果与对照组相比,氡吸入染毒组小鼠肺组织随着剂量的增加和染毒后时间的延续凋亡细胞逐渐增多;免疫组化结果显示,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p53蛋白表达量明显升高,在染毒后30d和90d时达到峰值;Bcl-2/Bax值则明显下降。结论氡染毒诱发小鼠肺细胞凋亡与p53和Bcl-2/Bax通路密切相关。Objective To study the mechanism of apoptasis by radon in lung tissue of mice.Methods Male BALB/c mice were exposed to radon with the cumulative dose of 0.02,30 or 60 working level month（WLM） respectively,and then were raised for different time（24h、30d or 90d）.Apoptosis was detected by terminal deoxynucleotidy transferase-mediated dUTP-biotin nick end labeling（TUNEL）.The expression of p53 and Bcl-2/Bax protein was observed by immunohistochemistry.Results As compared with the control group,the apoptotic index in lung tissue increased along with the increasing of expose dose and the raise time.The protein expression of p53 increased significantlyin the 30d and 90d groups.But Bcl-2/Bax expression decreased.Conclusions The apoptosis by radon in lung tissue of mice had close relationship with p53 and.Bcl-2/Bax pathway.

关 键 词：氡 肺损伤 细胞凋亡 P53 BCL-2/BAX 

分 类 号：R285.5[医药卫生—中药学]