基于细菌毒性测试与小鼠肺基因转录分析的PM_(2.5)健康效应  

Health Effects of PM_(2.5) Based on Bacterial Toxicity Test and Transcriptional Analysis in Lungs of Mice

作　　者：宋鹏程[1] 陆书玉[1,2] 魏永杰 陈晓倩[4] 罗丽娟[5] SONG Peng-cheng1, LU Shu-yu1,2 , WEI Yong-jie 3, CHEN Xiao-qian4, LUO Li-juan5(1. College of Environmental Science and Engineering, Donghua University, Shanghai 201620, China; 2. Shanghai Society of Environmental Sciences, Shanghai 200003, China; 3. Chinese Research Academy of Environmental Sciences, Beijing 100012, China; 4. Shanghai Academy of Public Measurement, Shanghai 201203, China; 5. Shanghai Radio-Environment Supervision Agency, Shanghai 200065, Chin)

机构地区：[1]东华大学环境科学与工程学院,上海201620 [2]上海市环境科学学会,上海200003 [3]中国环境科学研究院,北京100012 [4]上海市检测中心,上海201203 [5]上海市辐射环境监督站,上海200065

出　　处：《环境科学》2018年第5期2489-2497,共9页Environmental Science

基　　金：上海市环境保护局环保科研项目专项(沪环科2013第79号;沪环科2014第38号)

摘　　要：尽管大量流行病学和毒理学研究表明,PM_(2.5)暴露会导致一系列肺部疾病,但是其毒性机制尚不明确.本研究选取不同浓度梯度PM_(2.5)颗粒物样品进行细菌毒性评价,结果显示颗粒物的发光细菌急性毒性、遗传毒性分别为低毒和阴性.此外,采用气管灌注方法模拟小鼠呼吸暴露,研究了肺脏病理改变及差异基因表达.肺脏病理切片分析显示,PM_(2.5)暴露造成肺组织不同程度炎症反应和纤维化损伤,并呈现浓度越高、损伤程度越明显的现象.通路分析发现PM_(2.5)暴露影响到核糖体蛋白功能、脂肪酸与胆固醇代谢功能的正常表达,提示肺部炎症反应源于基因损害,其造成的损害后果可能是不可逆的.GO聚类分析发现免疫功能发生聚类富集,相关基因功能异常表达可能是造成肺部炎症的具体路径.这些发现有助于了解PM_(2.5)暴露危害路径和机制.Although epidemiology and toxicology studies have demonstrated that exposure to ambient air particles could result in a variety of lung diseases,but the pulmonary toxicological mechanism remains obscure. In this study,the toxicity of PM2.5 particles in different concentrations was investigated by toxicological methods,including the luminescent bacteria acute toxicity test and genotoxicity performed by SOS chromogenic reaction. The results indicated that,the acute toxicity and genotoxicity were low and negative,respectively. In addition,rats were treated with PM（2.5） suspension through intratracheal instillation,and the pathologic changes and expression of different genes in their lungs were carried out. We found that PM（2.5） exposure resulted in fibrotic changes and inflammation in the lung with the increase in PM（2.5） concentration. Pathway analysis indicated that PM（2.5） can induce pulmonary toxicity through disturbing the function of ribosomal protein,fatty acids,and cholesterol metabolism,suggesting an inflammatory reaction in the lung is caused by genetic damage and is irreversible. A gene ontology analysis revealed that abnormal expression of related genes in the immune response could be the specific pathway of lung inflammation. These findings improve our understanding of the toxicological pathway and mechanism of PM（2.5） exposure.

关 键 词：PM2.5 急性毒性 遗传毒性 转录组分析 差异基因 

分 类 号：X171.5[环境科学与工程—环境科学]