汽油尾气对人肺腺癌A549细胞的氧化损伤效应研究

为研究汽油燃烧汽车尾气(简称汽油尾气)的氧化损伤效应及其可能的毒作用机制,以人肺腺癌A549细胞为研究对象,采用MTT试验测试汽油尾气对细胞的毒性作用;通过测定细胞内超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性了解细胞在汽油尾气作用下抗氧化水平的改变;并用彗星试验检测汽油尾气对细胞DNA氧化损伤及修复的影响．结果显示汽油尾气在浓度≥0．0625L·mL-1时即显示出明显的细胞毒性;汽油尾气作用下A549 细胞SOD及GSH-Px活性均下降,在一定的浓度范围内与对照组比较有统计学差异(p<0．05)．汽油尾气可诱导 A549细胞不同程度的DNA氧化损伤,且细胞拖尾率和DNA迁移长度均随着汽油尾气浓度的增加而增加;损伤后 A549细胞修复发生较快,3小时内基本修复完全．提示汽油尾气具有明显的细胞毒性作用,可影响A549细胞抗氧化酶活性,并可导致DNA的氧化损伤．

Oxidative Damage Induced by Extract from Gasoline-fueled Vehicle Emissions in Human Lung Adenocarcinoma A549 Cells

Human lung adenocarcinoma A549 cell was used to investigate the oxidative damage induced by extract from gasoline-fueled vehicle emissions (gasoline emissions for short) in human. The cytotoxicity of gasoline emissions was detected by MTT test. The antioxidative ability was evaluated by detecting the activity of SOD and GSH-Px in cells. And comet assay was used to detect DNA damage and repair. Obvious cytotoxicity was showed when the concentration of gasoline emissions ≥0,0625L ·mL-1. SOD and GSH-Px activity decreased significantly after treatment with gasoline emissions. And gasoline emissions could also induce oxidative DNA damage in A549 cell. The rate of comet cells and DNA migration length increased with the increase of concentration. The DNA repair began early after remove of gasoline emissions and finished basically within 3h. The results suggested that gasline emissions had obvious citotoxicity, and could impair antioxidative ability of A549 cells as well as induced oxidative DNA damage in A549 cells.