Water soluble and insoluble components of PM2.5 and their functional cardiotoxicities on neonatal rat cardiomyocytes in vitro
Water soluble and insoluble components of PM2.5 and their functional cardiotoxicities on neonatal rat cardiomyocytes in vitro
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PM2.5水溶性和不溶性成分及其对体外新生大鼠心肌细胞的功能性心脏毒性
DOI：
10.1016/j.ecoenv.2018.10.107
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发表时间：
2019
影响因子：
6.8
通讯作者：
Cai Zongwei
中科院分区：
文献类型：
--
作者：
Qi Zenghua;Song Yuanyuan;Ding Qianqian;Liao Xiaoliang;Li Ruijin;Liu Guoguang;Tsang SukYing;Cai Zongwei
越来越多的流行病学调查表明，PM2.5是大气污染导致心血管功能障碍的重要促进因素。PM2.5是一种由固体和液体悬浮颗粒物组成的复杂混合物，其组成成分在很大程度上决定了PM2.5的健康风险。然而，不同的PM2.5组分的个体心脏毒性仍然不清楚，特别是在细胞水平上。本研究采用新生大鼠心肌细胞（NRCMs）评价PM2.5暴露对心脏的毒性作用。采用体外细胞毒性试验，研究了总PM2. 5、PM2. 5水溶性组分（WS-PM2.5）和PM2. 5水不溶性组分（WIS-PM2.5）对NRCMs的细胞毒性，包括细胞活力、细胞膜损伤和活性氧（ROS）产生。结果表明，当总PM2. 5或WIS-PM2. 5浓度高于50 μg/mL时，NRCM细胞活力显著降低，细胞膜损伤明显，ROS水平显著升高。当WS-PM 2. 5浓度升高至75 μg/mL时，其对NRCM细胞的毒性作用开始增强。此外，在暴露于Total-PM2.5、WS-PM2. 5或WIS-PM2.5（75 μg/mL）48 h后，检测到NRCM中的DNA损伤，并且仅在Total-PM2. 5和WIS-PM2. 5处理组中检测到对NRCM的线粒体功能和动作电位的不利影响。综上所述，我们的项目不仅评估了PM2. 5对心肌细胞的风险，而且揭示了总PM2. 5和WIS-PM2. 5暴露主要与NRCM的功能性心脏毒性相关。
A growing number of epidemiological surveys show that PM2.5is an important promoter for the cardiovascular dysfunction induced by atmospheric pollution. PM2.5is a complex mixture of solid and liquid airborne particles and its components determine the health risk of PM2.5to a great extent. However, the individual cardiotoxicities of different PM2.5fractions are still unclear, especially in the cellular level. Here we used the neonatal rat cardiomyocytes (NRCMs) to evaluate the cardiac toxicity of PM2.5exposure. The cytotoxicities of Total-PM2.5, water soluble components of PM2.5(WS-PM2.5) and water insoluble components of PM2.5(WIS-PM2.5), which include the cell viability, cell membrane damage, reactive oxygen species (ROS) generation, were examined with NRCMs in vitro. The results indicated that Total-PM2.5or WIS-PM2.5exposure 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-PM2.5exposure could induce the cytotoxicity on NRCMs until the concentration of WS-PM2.5was raised to a higher concentration (75 µg/mL). Furthermore, the DNA damage was detected in NRCMs after 48 h of exposure with Total-PM2.5, WS-PM2.5or WIS-PM2.5(75 µg/mL) and the adverse effects on mitochondrial function and action potentials of NRCMs were detected only both in the Total-PM2.5and WIS-PM2.5treatment group. In summary, our project not only estimates the risk of PM2.5on cardiac cells but also reveal that Total-PM2.5and WIS-PM2.5exposure were predominantly associated with the functional cardiotoxicities in NRCMs.