植物系统和人体细胞体外监测城市空气颗粒物(PM 2.5和PM 10组分)的遗传毒性:比较分析。

A. Poma, L. Arrizza, Pietro Picozzi, L. Spanò
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引用次数: 19

摘要

由心肺并发症引起的死亡率和发病率的增加与空气动力学直径为10微米(PM 10)和2.5微米(PM 2.5)的城市空气颗粒(UAP)水平升高有关。在本报告中,替代植物系统和体外人类细胞与UAP的人类危害和遗传毒性风险评估有关。利用胡萝卜和hs27人成纤维细胞悬浮液和玉米根分生组织的体外模型,通过评估微核诱导和/或姐妹染色单体交换(SCE),分析了空气中粗粒(pm10)和细粒(PM 2.5)的遗传毒性活性。结果表明,测试系统的反应存在差异,并表明植物和人类细胞培养中的诱变趋势与空气中pm2.5颗粒中富碳颗粒的浓度直接相关。此外,在植物组织中,微核和SCE的频率与胁迫相关酶过氧化物酶的比活性增强有关。
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Monitoring urban air particulate matter (fractions PM 2.5 and PM 10) genotoxicity by plant systems and human cells in vitro: a comparative analysis.
Increased incidence of mortality and sickness due to cardiopulmonary complications has been associated with elevated levels of urban air particles (UAP), with an aerodynamic diameter of 10 microm (PM 10) and 2.5 microm (PM 2.5). In the present report alternative plant systems and human cells in vitro are associated with human hazard and genotoxic risk assessment of UAP. The genotoxic activities associated with the coarse (PM 10) and the fine fraction (PM 2.5) of airborne particulates have been analyzed by evaluating micronuclei induction and/or sister-chromatid exchange (SCE) using in vitro models of Daucus carota and HS 27 human fibroblast cell suspensions and Zea mays root meristems. Results show variability in the response of the test systems and indicate that the mutagenicity trend in both plant and human cell cultures was directly correlated to the concentration of carbon-rich particles in the fraction of the PM 2.5 airborne particulates. Moreover, in plant tissues, the frequency of micronuclei and SCE was related to an enhancement of the specific activity of the stress-related enzyme peroxidase.
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