活性氧在硒致HepG2 DNA损伤中的作用  

Role of reactive oxygen species in sodium selenite induced DNA damage in HepG2 cells

作　　者：邹云锋[1] 牛丕业[1] 宫智勇[1] 袁晶[1] 邬堂春[1] 陈学敏[1] 

机构地区：[1]华中科技大学同济医学院劳动卫生与环境卫生学系教育部环境与健康重点实验室,武汉430030

出　　处：《卫生研究》2006年第3期291-293,共3页Journal of Hygiene Research

基　　金：国家自然科学基金资助项目(No.30471431)

摘　　要：目的探讨亚硒酸钠(Na2SeO3)致HepG2细胞DNA损伤的作用机制。方法用0、2·5、5、10、20μmol/L的Na2SeO3、及分别加有还原性谷胱甘肽(GSH)和N-乙酰基-L-半胱氨酸(NAC)的Na2SeO3(10μmol/L)处理HepG2。用四甲基偶氮唑盐(MTT)比色法测定细胞活性;流式细胞仪测细胞内活性氧(ROS)的水平以及用彗星实验检测细胞的DNA损伤。结果5、10、20μmol/L Na2SeO3作用于HepG21h即引起ROS增加,12h后即导致细胞HepG2活性下降,24h后DNA损伤增强,与对照组相比,差异有统计学意义(P<0·05);抗氧化剂GSH和NAC有效抑制了ROS升高,并增强了细胞活性,减弱了细胞DNA损伤,与未加GSH和NAC的Na2SeO3组(10μmol/L)相比,差异有统计学意义(P<0·05)。结论ROS的产生可能是亚硒酸钠造成HepG2DNA损伤的重要原因。Objective To investigate the mechanisms of sodium selenite induced DNA damage in HepG2 cells. Methods HepG2 cells were treated with the designed concentrations of sodium selenite and the selenite （10μmol/L） added simultaneously with GSH （10mmol）and NAC （5mmol）. Then the cell viability was detected by MTT, and the flurescent intensity of reactive oxygen species（ROS） was determined by flow cytometry, and DNA damage was detected by commet assay. Results The level of ROS was increased after HepG2 was treated with 5,10,20μmol/L sodium selenite for one hour, and the cell viability was decreased after 12 hours, and the DNA damage was enhanced. Compared with the control group, the difference was statistically significant（ P 〈 0.05）. GSH and NAC effectively inhibited the ROS increased and cell viability decreased and DNA damage weakened. Conclusion ROS may be the important reason that sodium selenite induced HepG2 cells DNA damage.

关 键 词：活性氧 亚硒酸钠 DNA损伤 

分 类 号：R730.1[医药卫生—肿瘤] Q581[医药卫生—临床医学]