Institute of Environmental Health and Pollution Control, School of Environmental Science and Engineering, Guangdong University of Technology, Guangzhou, Guangdong, China.
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China.
Ecotoxicol Environ Saf. 2019 Jan 30;168:378-387. doi: 10.1016/j.ecoenv.2018.10.107. Epub 2018 Nov 2.
A growing number of epidemiological surveys show that PM is an important promoter for the cardiovascular dysfunction induced by atmospheric pollution. PM is a complex mixture of solid and liquid airborne particles and its components determine the health risk of PMto a great extent. However, the individual cardiotoxicities of different PM fractions are still unclear, especially in the cellular level. Here we used the neonatal rat cardiomyocytes (NRCMs) to evaluate the cardiac toxicity of PM exposure. The cytotoxicities of Total-PM, water soluble components of PM (WS-PM) and water insoluble components of PM (WIS-PM), which include the cell viability, cell membrane damage, reactive oxygen species (ROS) generation, were examined with NRCMs in vitro. The results indicated that Total-PM or WIS-PM exposure significantly decreased the cell viability, induced the cell membrane damage and increased the ROS level in NRCMs at concentrations above 50 µg/mL. However, WS-PM exposure could induce the cytotoxicity on NRCMs until the concentration of WS-PM was raised to a higher concentration (75 µg/mL). Furthermore, the DNA damage was detected in NRCMs after 48 h of exposure with Total-PM, WS-PM or WIS-PM (75 µg/mL) and the adverse effects on mitochondrial function and action potentials of NRCMs were detected only both in the Total-PM and WIS-PM treatment group. In summary, our project not only estimates the risk of PM on cardiac cells but also reveal that Total-PM and WIS-PM exposure were predominantly associated with the functional cardiotoxicities in NRCMs.
越来越多的流行病学调查表明，PM 是大气污染引起心血管功能障碍的重要促进剂。PM 是固体和液体空气颗粒的复杂混合物，其成分在很大程度上决定了 PM 对健康的风险。然而，不同 PM 组分的个体心脏毒性仍不清楚，尤其是在细胞水平。在这里，我们使用新生大鼠心肌细胞（NRCMs）来评估 PM 暴露的心脏毒性。用 NRCMs 体外检测了总 PM、PM 的水溶性成分（WS-PM）和 PM 的水不溶性成分（WIS-PM）的细胞活力、细胞膜损伤、活性氧（ROS）生成等细胞毒性。结果表明，总 PM 或 WIS-PM 暴露在浓度高于 50μg/mL 时，显著降低了 NRCMs 的细胞活力，诱导了细胞膜损伤，并增加了 ROS 水平。然而，WS-PM 暴露在浓度升高到更高浓度（75μg/mL）时，才会对 NRCMs 产生细胞毒性。此外，在总 PM、WS-PM 或 WIS-PM（75μg/mL）暴露 48 小时后，NRCMs 中检测到 DNA 损伤，只有在总 PM 和 WIS-PM 处理组中才检测到对 NRCMs 线粒体功能和动作电位的不良影响。总之，我们的项目不仅评估了 PM 对心脏细胞的风险，还揭示了总 PM 和 WIS-PM 暴露主要与 NRCMs 的功能心脏毒性有关。
