收稿日期: 2016-01-12
网络出版日期: 2016-04-30
基金资助
国家自然科学基金资助项目(21107068, 41561144007);上海大学长江学者和创新团队发展计划资助项目(IRT13078)
Combined effects of 1-nitropyrene and benzo(a)pyrene on cytotoxicity and DNA damage in human lung epithelial A549 cells
1-硝基芘(1-nitropyrene, 1-NP)是柴油车尾气中检测浓度最高的硝基多环芳烃. 以1-NP 为主体, 人肺上皮A549 细胞为研究对象, 探讨了1-NP 和苯并[a] 芘(benzo(a)pyrene, B[a]p)的联合细胞毒性及其对DNA 的损伤. 联合染毒实验结果表明: 当B[a]p 和1-NP 同时作用于A549 细胞时, B[a]p 能明显减弱由1-NP 造成的细胞增殖抑制和细胞内活性氧簇(reactive oxygen species, ROS)水平升高, 但对DNA 的损伤与1-NP 单独染毒组相近;利用B[a]p 预染毒A549 细胞24 h, 能明显减弱由1-NP 造成的细胞增殖抑制和ROS 水平升高, 但对DNA 的损伤加剧. 以上结果说明, 1-NP 和B[a]p 联合作用可能是通过抑制ROS 的生成来降低对细胞增殖的抑制, 但所造成的对DNA 损伤的加剧可能是通过其他的作用途径.
尚羽, 周倩, 蒋玉婷 . 1-硝基芘和苯并[a] 芘对人肺上皮A549 细胞的联合细胞毒性[J]. 上海大学学报(自然科学版), 2016 , 22(2) : 181 -187 . DOI: 10.3969/j.issn.1007-2861.2016.01.008
Using human lung epithelial A549 cells, combined toxic effects of 1-nitropyrene (1-NP) and benzo(a)pyrene (B[a]p) were evaluated. The 1-NP caused a significantly concentration-dependent viability decrease, DNA damage and reactive oxygen species (ROS) generation. Compared with the groups treated with 1-NP alone, viability was significantly increased and ROS generation was significantly reduced in combined-treated groups with 1-NP and B[a]p. However, the DNA damage was significantly increased in the combinedtreated groups compared with the groups treated with 1-NP alone. These results suggested that 1-NP may mediate the cytotoxic effects through ROS generation, and pretreatment, with B[a]p may inhibit ROS generation induced by 1-NP, and thereby reducing the cell death in A549 cells. However mechanisms of DNA damage deserves further investigations.
[1] 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.
[2] Halonen J I, Lanki T, Yli-Tuomi T, et al. Particulate air pollution and acute cardiorespiratory hospital admissions and mortality among the elderly [J]. Epidemiology, 2009, 20(1): 143-153.
[3] Kan H, London S J, Chen G, et al. Season, sex, age, and education as modifiers of the effects of outdoor air pollution on daily mortality in Shanghai, China: the public health and air pollution in Asia (PAPA) study [J]. Environmental Health Perspectives,2008, 116(9): 1183-1188.
[4] P¨oschl U. Atmospheric aerosol: composition, transformation, climate and health effects [J]. Angewandte Chemie International Edition in English, 2005, 44(46): 7520-7540.
[5] Bonnefoy A, Chiron S, Botta A. Environmental nitration processes enhance the mutagenic potency of aromatic compounds [J]. Environmental Toxicology, 2012, 27(6): 321-331.
[6] 王帮进, 李怀建, 占洁, 等.大气气溶胶中硝基多环芳烃分析方法的建立及应用[J].环境科学学报, 2011, 31(8): 1745-1749.
[7] Kucab J E, Phillips D H, Arlt V M. Metabolic activation of diesel exhaust carcinogens in primary and immortalized human TP53 knock-in (Hupki) mouse embryo fibroblasts [J]. Environmental and Molecular Mutagenesis, 2012, 53(3): 207-217.
[8] 尚羽, 蒋玉婷, 张玲, 等. 1-硝基芘和1,2-萘醌的联合细胞毒性和致DNA 损伤[J]. 环境科学, 2014, 35: 4345-4351.
[9] Park E J, Park K. Induction of pro-inflammatory signals by 1-nitropyrene in cultured BEAS-2B cells [J]. Toxicology Letters, 2009, 184(2): 126-133.
[10] Tice R R, Agurelle E, Anderson D, et al. Single cell gel/comet assay: guidelines for in vitro and in vivo genetic toxicology testing [J]. Environmental and Molecular Mutagenesis,
2000, 35(3): 206-221.
[11] 尚羽, 张玲, 范兰兰, 等. 大气颗粒物对A549 和HUVEC的DNA损伤机制[J]. 上海大学学报: 自然科学版, 2013, 19(4): 411-416.
[12] 范兰兰, 尚羽, 张玲. 大气颗粒物对A549 和HUVECs 细胞的毒性作用[J]. 环境科学研究, 2012,25(10): 101-107.
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