Abstract：ObjectiveTo investigate the cytotoxicity and oxidative stress of ambient fine particulate matter (PM2.5) and water-soluble fraction of PM2.5 on human bronchial epithelial cells (HBE ). MethodsPM2.5 samples were collected in the urban area of Hangzhou. Then the water-soluble fraction was extracted from PM2.5. After HBE cells were exposed to PM2.5 and its water-soluble fraction at the doses of 0, 100, 250, 500, 1 000, 1 500 and 2 000 μg/mL for 24 h, CCK-8 (cell counting kit-8 )assay was conducted to examine the cytotoxicity of the PM2.5 and its water-soluble fraction. The oxidative damage induced by PM2.5 and its water-soluble fraction on HBE cells was then evaluated with lipid peroxidation, the superoxide dismutase (SOD) activity, and the levels of glutathione peroxidase (GSH-Px). ResultsThe PM2.5 and its water-soluble fraction reduced the viability of HBE cells in a dose-dependent manner. When the PM concentrations were 200, 400 and 800 μg/mL, the SOD activity of the HBE cells decreased significantly, as compared with the control group (P< 0.05). Also, the malondialdehyde (MDA) levels of the HBE cells significantly increased at the doses of 200, 400 and 800 μg/mL (P< 0.05). However, there were no significant differences of GSH-Px activity among the groups. ConclusionThe PM2.5 and its water-soluble fraction could induce cytotoxic and oxidative damage effects on the HBE cells.
张世鑫, 伍立志, 陈苘, 郑云燕, 蔡德雷. 大气细颗粒物及其水提物对人支气管上皮细胞的氧化损伤效应[J]. 预防医学, 2016, 28(4): 332-335,339.
ZHANG Shi-xin, WU Li-zhi, CHEN Qing, ZHENG Yun-yan, CAI De-lei. A study on the oxidative stress induced by ambient fine particulate matter (PM2.5) and water-soluble fraction on HBE cells. Preventive Medicine, 2016, 28(4): 332-335,339.
[1] LU F, XU D, CHENG Y, et al. Systematic review and meta-analysis of the adverse health effects of ambient PM2.5 and PM 10 pollution in the Chinese population[J]. Environ Res, 2015(136): 196-204. [2] 中华人民共和国环境保护部. 2013中国环境状况公报[R].2014: 22-23. [3] DENG X, ZHANG F, WANG L, et al. Airborne fine particulate matter induces multiple cell death pathways in human lung epithelial cells[J]. Apoptosis, 2014, 19(7): 1099-1112. [4] WYZGA R E, ROHR A C. Long-term particulate matterexposure: Attributing health effects to individual PM components[J]. J Air Waste Manag Assoc, 2015, 65(5): 523-543. [5] 张少丹, 李武平. 呼吸道上皮细胞模型的研究进展[J]. 病毒学报, 2015, 31(3): 312-317. [6] USEPA. Integrated science assessment for particulate matter. Washington, DC: EPA, 2009. [7] HAN W, DAN W, SHUO Y, et al. Oxidative stress induced by urban fine particles in cultured EA.hy926 cells[J]. Hum Exp Toxicol, 2011, 30(7): 579-590. [8] 陈苘, 邹华, 邢鸣鸾, 等. 不同粒径纳米二氧化钛对大鼠氧化应激的影响[J]. 浙江预防医学, 2012, 24(11): 1-3. [9] 王菲菲, 王先良, 刘芳盈, 等. 燃煤PM2.5不同组分对血管内皮细胞的氧化损伤效应[J]. 中国环境科学, 2014(3): 780-785. [10] ZHANG Z G, NIU X Y, HE X J, et al. Ginsenoside rg1 reduces toxicity of fine particulate matter on human alveolar epithelial cells: A preliminary observation[J]. Mol Med Rep, 2014, 9(3): 989-992. [11] 董亮, 何永志, 王远亮, 等. 超氧化物歧化酶(SOD)的应用研究进展[J]. 中国农业科技导报, 2013(5): 53-58. [12] OKUBO T, HOSAKA M, NAKAE D. In vitro effects induced by diesel exhaust at an air-liquid interface in a human lung alveolar carcinoma cell line A549[J]. Exp Toxicol Pathol, 2015, 67(2015):383-388. [13] MICHAEL S, MONTAG M, DOTT W. Pro-inflammatory effects and oxidative stress in lung macrophages and epithelial cells induced by ambient particulate matter[J]. Environ Pollut, 2013(183): 19-29. [14] 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]. Environ Toxicol, 2014, in press. doi:10.1002/tox.22102. [15] HATZIS C, GODLESKI J J, GONZALEZ-FLECHA B, et al. Ambient particulate matter exhibits direct inhibitory effects on oxidative stress enzymes[J]. Environ Sci Technol, 2006, 40(8): 2805-2811. [16] 于扬, 魏景艳. 谷胱甘肽过氧化物酶及其合成机制[J]. 生物物理学报, 2013, 29(10): 724-737. [17] YI S, ZHANG F, QU F, et al. Water-insoluble fraction of airborne particulate matter (PM 10 ) induces oxidative stress in human lung epithelial A549 cells[J]. Environ Toxicol, 2014, 29(2): 226-233.
