采集北京市海淀区大气颗粒物粗颗粒(PM10−2.5)、细颗粒( PM2.5−0.1 ) 和超细颗粒(PM0.1),分析颗粒物对人肺上皮细胞(human lung epithelial cell, A549) 和人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVEC)的基因毒性及促进活性氧自由基(reactive oxygen species, ROS) 生成的机制. 彗星实验发现: PM10−2.5, PM2.5−0.1 和PM0.1 对2 种细胞均有显著的基因毒性, 并呈剂量-效应关系; 细和超细颗粒造成的DNA 损伤显著高于粗颗粒; HUVEC 细胞的DNA 损伤程度大于A549 细胞; PM2.5−0.1 和PM0.1 可诱导2 种细胞内ROS 水平显著升高, 而PM10−2.5 不能. 因此细胞内DNA 损伤可能与ROS 生成有一定联系.
Ambient particulate matter has become one of the most harmful pollutants in the air. The genotoxic effects and generationmechanism of reactive oxygen species (ROS) were studied in A549 and HUVEC cells treated with three sizes of ambient particles, PM10−2.5, PM2.5−0.1 and PM0.1. The results from comet assay show that PM10−2.5, PM2.5−0.1 and PM0.1 caused significant DNA damages in both A549 and HUVEC cells in a dose-dependent manner. In both types of cells, the DNA damage caused by PM2.5−0.1 and PM0.1are significantly higher than that caused by PM10−2.5, and PMs cause higher DNA damage in HUVEC cells than that in A549 cells. PM2.5−0.1 and PM0.1 can significantly increase the intracellular ROS level, but PM10−2.5 cannot. DNA damage in cells induced by particles may be related to the generation of ROS, which deserves further investigations.
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