引用本文:
魏舒婷, 姬晓彤, 岳慧峰, 李广科, 桑楠. PM2.5诱导人支气管上皮细胞线粒体损伤[J]. 环境化学, 2018, 37(9): 1895-1900
WEI Shuting, JI Xiaotong, YUE Huifeng, LI Guangke, SANG Nan. PM2.5 induced mitochondrial injury of Human Bronchial Epithelial Cells[J]. Environmental Chemistry, 2018, 37(9): 1895-1900

PM2.5诱导人支气管上皮细胞线粒体损伤
魏舒婷, 姬晓彤, 岳慧峰, 李广科, 桑楠
山西大学环境与资源学院, 太原, 030006
摘要:
流行病学和实验研究表明,PM2.5会对呼吸系统造成损害,但毒性机制还有待深入探讨.本研究采集太原市冬季PM2.5,考察其对人支气管上皮细胞(BEAS-2B细胞)的线粒体损伤效应.结果表明,PM2.5会造成细胞线粒体结构变化和功能异常,主要表现为三磷酸腺苷(ATP)水平和线粒体膜电位(MMP)随着PM2.5浓度升高而下降.此外,线粒体功能相关因子PGC-1α、NRF-1和TFAM的蛋白表达量也随着PM2.5浓度的升高呈下降趋势,并在30 μg·mL-1时达到最小值.这些结果提示,PM2.5可以导致BEAS-2B细胞发生线粒体结构和功能性变化,进而诱发呼吸系统损伤.
关键词:    PM2.5    呼吸系统    人支气管上皮细胞(BEAS-2B)    线粒体损伤   
PM2.5 induced mitochondrial injury of Human Bronchial Epithelial Cells
WEI Shuting, JI Xiaotong, YUE Huifeng, LI Guangke, SANG Nan
College of Environment and Resource, Shanxi University, Taiyuan, 030006, China
Abstract:
A large number of epidemiological and experimental studies have shown that PM2.5 could induce adverse effects on the respiratory system, but the toxicity mechanism remains to be unclear. Therefore, human bronchial epithelial cells (BEAS-2B cells) were exposed to the winter PM2.5 of Taiyuan. The results showed that PM2.5 exposure induced abnormal changes on mitochondria structure and function, such as decreased levels of adenosine triphosphate (ATP) content and the mitochondrial membrane potential (MMP) of the cells with the increase of PM2.5 concentration. In addition, the protein expression of PGC-1α, NRF-1 and TFAM was also decreased, and reached the minimum when PM2.5 concentration was 30 μg·mL-1. These results suggested that PM2.5 could induce structural and functional changes of mitochondria in BEAS-2B cells, which could lead to respiratory injury.
Key words:    PM2.5    respiratory system    BEAS-2B    mitochondria   
收稿日期: 2017-11-09
基金项目: 国家自然科学基金(21477070,91543203),山西省青年三晋学者支持计划和山西省高等学校优秀创新团队支持计划资助.
李广科,Tel:03517011932,E-mail:liguangke@sxu.edu.cn
相关功能
PDF(6639KB) Free
打印本文
加入收藏夹
把本文推荐给朋友
作者相关文章
魏舒婷  在本刊中的所有文章
姬晓彤  在本刊中的所有文章
岳慧峰  在本刊中的所有文章
李广科  在本刊中的所有文章
桑楠  在本刊中的所有文章

参考文献:
[1] POPE C A, DOCKERY D W. Health effects of fine particulate air pollution: lines that connect[J]. Journal of the Air & Waste Manage Association, 2006, 56(6): 709-742.
[2] MAKKONEN U, HELLÉN H, ANTTILA P, et al. Size distribution and chemical composition of airborne particles in south-eastern Finland during different seasons and wildfire episodes in 2006[J]. Science of the Total Environment, 2010, 408(3): 644-651.
[3] POPE C A, BURNETT R T,THUN M J, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution[J]. The Journal of the American Medical Association, 2002, 287(9): 1132-1141.
[4] CORREIA A W, POPE C A, DOCKERY D W, et al. Effect of air pollution control on life expectancy in the United States: an analysis of 545 U.S. counties for the period from 2000 to 2007[J]. Epidemiology, 2013, 24(1): 23-31.
[5] HWANG S L, GUO S E, CHI M C, et al. Association between atmospheric fine particulate matter and hospital admissions for chronic obstructive pulmonary disease in southwestern Taiwan: A population-based study[J]. International Journal of Environmental Research and Public Health, 2016, 13(4): 366.
[6] NI L, CHUANG C C, ZUO L. Fine particulate matter in acute exacerbation of COPD[J]. Frontiers in Physiology, 2015, 6: 294.
[7] HAMRA G B, GUHA N, COHEN A, et al. Outdoor particulate matter exposure and lung cancer: A systematic review and meta-analysis[J]. Environmental Health Perspectives, 2014, 122(9): 906-911.
[8] FAN J C, LI S L, FAN C L, et al. The impact of PM2.5 on asthma emergency department visits: A systematic review and meta-analysis[J]. Environmental Science and Pollution Research International, 2016, 23(1): 843-850.
[9] TSAI S S, YANG C Y. Fine particulate air pollution and hospital admissions for pneumonia in a subtropical city: Taipei, Taiwan[J]. Journal of Toxicology and Environmental Health. Part A, 2014, 77(4): 192-201.
[10] LAI T C, CHIANG C Y, WU C F, et al. Ambient air pollution and risk of tuberculosis: A cohort study[J]. Occupational and Environmental Medicine, 2016, 73(1): 56-61.
[11] RIVA D R, MAGALHÃES C B, LOPES A A, et al. Low dose of fine particulate matter (PM2.5) can induce acute oxidative stress, inflammation and pulmonary impairment in healthy mice[J]. Inhalation Toxicology, 2011, 23(5): 257-267.
[12] 翟中和,王喜忠,丁明孝. 细胞生物学(第三版)[M]. 北京: 高等教育出版社,2007. ZHAI Z H, WANG X Z, DING M X, et al. Cell biology (Third Edition)[M]. Beijing: Higher Education Press, 2007 (in Chinese).
[13] ZHAO Q, CHEN H, YANG T, et al. Direct effects of airborne PM2.5 exposure on macrophage polarizations[J]. Biochimica et Biophysica Acta, 2016, 1860(12): 2835-2843.
[14] LI R, KOU X, GENG H, et al. Effect of ambient PM2.5 on lung mitochondrial damage and fusion/fission gene expression in rats[J]. Chemical Research in Toxicology, 2015, 28(3): 408-418.
[15] SOBERANES S, URICH D, BAKER C M, et al. Mitochondrial complex Ⅲ-generated oxidants activate ASK1 and JNK to induce alveolar epithelial cell death following exposure to particulate matter air pollution[J]. The Journal of Biological Chemistry, 2009, 284(4): 2176-2186.
[16] JI X, KU T, ZHU N, et al. Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism[J]. Journal of Hazardous Materials, 2016, 320: 176-186.
[17] ZHANG Y, ZHENG L, TUO J, et al. Analysis of PM2.5-induced cytotoxicity in human HaCaT cells based on a microfluidic system[J]. Toxicology in vitro, 2017, 43: 1-8.
[18] VUONG N Q, BREZNAN D, GOEGAN P, et al. In vitro toxicoproteomic analysis of A549 human lung epithelial cells exposed to urban air particulate matter and its water-soluble and insoluble fractions[J]. Particle and Fibre Toxicology, 2017, 14(1): 39.
[19] THOMSON E M, BREZNAN D, KARTHIKEYAN S, et al. Cytotoxic and inflammatory potential of size-fractionated particulate matter collected repeatedly within a small urban area[J]. Particle and Fibre Toxicology, 2015, 12: 24.
[20] MAGNANI N D, MARCHINI T, VANASCO V, et al. Reactive oxygen species produced by NADPH oxidase and mitochondrial dysfunction in lung after an acute exposure to residual oil fly ashes[J]. Toxicology and Applied Pharmacology, 2013, 270(1): 31-38.
[21] YANG L, LIU G, LIN Z, et al. Pro-inflammatory response and oxidative stress induced by specific components in ambient particulate matter in human bronchial epithelial cells[J]. Environmental Toxicology, 2016, 31(8): 923-936.
[22] SCARPULLA R C. Nuclear activators and coactivators in mammalian mitochondrial biogenesis[J]. Biochimica et Biophysica Acta, 2002, 1576(1-2): 1-14.
[23] KANG D, KIM SH, HAMASAKI N. Mitochondrial transcription factor A (TFAM): roles in maintenance of mtDNA and cellular functions[J]. Mitochondrion, 2007, 7(1-2): 39-44.
[24] 阎德民,王伟,王波,等. 温度对PGC-1在心肌细胞中表达的影响[J]. 中国医科大学学报,2008,37 (1):38-40. YAN D M, WANG W, WANG B, et al. The expression of PGC-1 in the heart in vitro in different temperature[J]. Journal of China Medical University, 2008, 37(1): 38-40 (in Chinese).
[25] 秦国华,武美琼,桑楠. SO2和BaP复合暴露诱导小鼠肺线粒体损伤的分子机制[J]. 中国环境科学,2015,35(11):3496-3501. QIN G H, WU M Q, SANG N. Molecular mechanism of co-exposure of sulfur dioxide and benzo(a)pyrene on mouse pulmonary cell mitochondria damage[J]. China Environmental Science, 2015, 35(11): 3496-3501 (in Chinese).
[26] ZHANG L, BAO Y, LIU Y, et al. Downregulation of nuclear respiratory factor-1 contributes to mitochondrial events induced by benzo(a)pyrene[J]. Environmental Toxicology, 2014, 29(7): 780-787.