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首页> 外文期刊>Environmental toxicology >Water-Insoluble Fraction of Airborne Particulate Matter (PM_(10)) Induces Oxidative Stress in Human Lung Epithelial A549 Cells
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Water-Insoluble Fraction of Airborne Particulate Matter (PM_(10)) Induces Oxidative Stress in Human Lung Epithelial A549 Cells

机译:航空颗粒物(PM_(10))的水不溶性分数诱导人肺上皮A549细胞的氧化应激

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摘要

Exposure to ambient airborne participate matter (PM) with an aerodynamic diameter less than 10 μm (PM_(10)) links with public health hazards and increases risk for lung cancer and other diseases. Recent studies have suggested that oxidative stress is a key mechanism underlying the toxic effects of exposure to PM_(10). Several components of water-soluble fraction of PM_(10) (sPM_(10)) have been known to be capable of inducing oxidative stress in in vitro studies. In this study, we investigated if water-insoluble fraction of PM_(10) (iPM_(10)) could be also capable of inducing oxidative stress and oxidative damage. Human lung epithelial A549 cells were exposed to 10 μg/mL of sPM_(10), iPM_(10) or total PM_(10) (tPM_(10)) preparation for 24 h. Here, we observed that all three PM_(10) preparations reduced cell viability and induced apoptotic cell death in A549 cells. We further found that, similar to the exposure to sPM_(10) and tPM_(10), the intracellular level of hydrogen peroxide (H_2O_2) in the iPM_(10)-exposed cells was increased significantly; meanwhile the activity of catalase was decreased significantly as compared with the unexposed control cells, resulting in significant DNA damage. Our data obtained from inductively coupled plasma-mass spectrometry (ICP-MS) assays showed that iron is the most abundant metal in all three PM_(10) preparations. Thus, we have demonstrated that, similar to sPM_(10), iPM_(10) is also capable of inducing oxidative stress by probably inducing generation of H_2O_2 and impairing enzymatic antioxidant defense, resulting in oxidative DNA damage and even apoptotic cell death through the iron-catalyzed Fenton reaction.
机译:暴露于空气动力学直径小于10μm(PM_(10))的周围空气传播参与物(PM)会危害公共健康,并增加患肺癌和其他疾病的风险。最近的研究表明,氧化应激是暴露于PM_(10)的毒性作用的关键机制。在体外研究中,已知PM_(10)(sPM_(10))的水溶性部分的某些成分能够诱导氧化应激。在这项研究中,我们调查了PM_(10)(iPM_(10))的水不溶性部分是否也能够诱导氧化应激和氧化损伤。将人肺上皮A549细胞暴露于10μg/ mL的sPM_(10),iPM_(10)或总PM_(10)(tPM_(10))制剂中24小时。在这里,我们观察到所有三种PM_(10)制剂均降低了细胞活力,并诱导了A549细胞的凋亡。我们进一步发现,与暴露于sPM_(10)和tPM_(10)相似,暴露于iPM_(10)的细胞的细胞内过氧化氢(H_2O_2)水平显着增加;同时,与未暴露的对照细胞相比,过氧化氢酶的活性显着降低,导致DNA明显受损。我们从电感耦合等离子体质谱(ICP-MS)分析获得的数据表明,铁是所有三种PM_(10)制剂中含量最高的金属。因此,我们已经证明,与sPM_(10)相似,iPM_(10)也能够通过可能诱导H_2O_2生成并削弱酶促抗氧化防御能力来诱导氧化应激,从而导致氧化DNA损伤甚至通过铁使凋亡细胞死亡。 -催化的芬顿反应。

著录项

  • 来源
    《Environmental toxicology》 |2014年第2期|226-233|共8页
  • 作者单位

    Laboratory of Environment and Health, College of Life Sciences, Graduate University of the Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, People's Republic of China;

    Laboratory of Environment and Health, College of Life Sciences, Graduate University of the Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, People's Republic of China;

    Laboratory of Environment and Health, College of Life Sciences, Graduate University of the Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, People's Republic of China;

    Laboratory of Environment and Health, College of Life Sciences, Graduate University of the Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, People's Republic of China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    PM_(10); cytotoxicity; oxidative stress; apoptosis; DNA damage; lung epithelial cells;

    机译:PM_(10);细胞毒性氧化应激细胞凋亡DNA损伤;肺上皮细胞;

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