大气亚微米颗粒物对哺乳动物肺部毒性效应研究

On pulmonary toxicity of atmospheric submicron particles to mammals

为研究大气亚微米颗粒物(PM1)对哺乳动物肺部的毒性效应,采集杭州市区高架附近的PM1样品,分别对人正常肺上皮细胞(BEAS-2b)进行急性暴露,对ICR小鼠进行亚慢性暴露。结果表明,在PM1急性暴露后,BEAS-2b细胞活性受到明显的抑制,胞内ROS水平显著上升(p <0.05),SOD活性和GSH/GSSG比值显著下降(p <0.05),各指标均呈明显的剂量-效应关系,表明PM1具有明显的细胞毒性。在PM1亚慢性暴露下,ICR小鼠肺组织出现病理性变化,且组织内ROS水平显著上升,GSH/GSSG比值显著下降(p <0.05);与此同时,肺组织内炎性因子IL-6、IL-7及TNF-α的含量显著增加(p <0.05),抗炎因子IL-10的含量显著降低(p <0.05),各指标均呈明显的剂量-效应关系,该研究结果表明PM1亚慢性暴露可诱导ICR小鼠肺组织的的氧化损伤和炎症效应。

The given paper is inclined to collect and examine the atmospheric submicron particulates( PM1) nearby the highway regions in Hangzhou City to investigate their pulmonary toxicity to the mammals nearby. To achieve the purpose,we have performed acute exposure of PM1 to the normal human lung epithelial cells( BEAS-2 b) in a period of 24 h at the exposure concentration rates of 25 μg/mL,50 μg/mL,100 μg/mL,200 μg/mL and 400 μg/mL,correspondingly and respectively,in a contrastive way by setting up the control group. And,then,when the acute exposure to PM1 has been done,the exposure activity of BEAS-2 b cells should necessarily be given up. And,then,the median lethal concentration rate( LC50,24 h) of PM1 to BEAS-2 b cells has been assessed and confirmed to be 400 μg/mL.And,later,when compared to the control group,the ROS levels in the exposed cells have been found significantly increased( p <0. 05) whereas the SOD activity and GSH/GSSG ratio would be noticed significantly decreased( p < 0. 05). The above said results can obviously indicate the effect of the PM1 cytotoxicity.Furthermore,we have conducted the sub-chronical exposure of ICR mice to PM1,too,during the period of 60 days by an oral and nasal inhalation exposure system at the concentration rates of15 μg/m3,75 μg/m3 and 250 μg/m3,respectively,which had been lasting for 5 days in a week and 2 heachday in comparison to the control group. Through the subchronic exposure of PM1,the lung tissues of ICR mice has been found exhibiting the pathological changes,such as inflammatory cell infiltration and irregular arrangement of the alveolar cells. Furthermore,as compared to the control group,the ROS level in the lung tissues of exposed mice has been noticed grown up where as the ratio of GSH/GSSG has been found significantly decreased( p < 0. 05). And,additionally,the inflammatory factors including IL-6,IL-7 and TNF-α in the lung tissues of exposed mice have been turning to be significantly increased( p < 0. 05),though that of the anti-inflammatory factor IL-10 was noticed sharply decreased( p <0. 05). Hence,the above results tend to tell us that the subchronical exposure of PM1 can induce oxidative damage and consequently affect inflammatorily the lung tissues of the ICR mice.