Effects of Size-Fractionated Particulate Matter on Cellular Oxidant Radical Generation in Human Bronchial Epithelial BEAS-2B Cells.
Effects of Size-Fractionated Particulate Matter on Cellular Oxidant Radical Generation in Human Bronchial Epithelial BEAS-2B Cells.
复制标题
粒度分级颗粒物对人支气管上皮BEAS-2B细胞氧化自由基产生的影响
DOI：
10.3390/ijerph13050483
复制
发表时间：
2016-05-10
影响因子：
--
通讯作者：
Ding W
中科院分区：
文献类型：
--
作者：
Guan L;Rui W;Bai R;Zhang W;Zhang F;Ding W
本研究的目的是调查尺寸分级（即，<1;空气动力学直径为1-2.5和2.5-10 µm）环境颗粒物（PM）对人支气管上皮细胞（BEAS-2B）中活性氧（ROS）活性和细胞活力的影响。从2013年3月至2014年12月，从中国北京的城市站点（uPM）和鞍山的钢铁厂站点（sPM）收集PM样品。分析了uPM和sPM中的金属元素、有机碳和元素碳以及水溶性无机离子。MTS法和DCFH-DA法检测PM-BEAS-2B细胞活性和ROS生成量，结果表明uPM和sPM均使细胞活性降低，ROS生成量增加。在sPM1.0中测量的ROS水平大约是uPM1.0中的三倍。相关性分析结果表明，活性氧活性和细胞毒性与不同PM组分有关。此外，去铁胺（DFO）显着防止增加的ROS产生和细胞活力的下降。综上所述，我们的研究结果表明，PM上吸收的金属诱导BEAS-2B细胞产生氧化自由基，可能导致肺功能受损。
The aim of the present study was to investigate the effects of size-fractionated (i.e., <1; 1–2.5, and 2.5–10 µm in an aerodynamic diameter) ambient particulate matter (PM) on reactive oxygen species (ROS) activity and cell viability in human bronchial epithelial cells (BEAS-2B). The PM samples were collected from an urban site (uPM) in Beijing and a steel factory site (sPM) in Anshan, China, from March 2013 to December 2014. Metal elements, organic and elemental carbon, and water-soluble inorganic ions in the uPM and sPM were analyzed. The cell viability and ROS generation in PM-exposed BEAS-2B cells were measured by MTS and DCFH-DA. The results showed that both uPM and sPM caused a decrease in the cell viability and an increase in ROS generation. The level of ROS measured in sPM1.0 was approximately triple that in uPM1.0. The results of correlation analysis showed that the ROS activity and cytotoxicity were related to different PM composition. Moreover, deferoxamine (DFO) significantly prevented the increase of ROS generation and the decrease of cell viability. Taken together, our results suggest that the metals absorbed on PM induced oxidant radical generation in BEAS-2B cells that could lead to impairment of pulmonary function.