TY - JOUR
T1 - Water soluble and insoluble components of PM2.5 and their functional cardiotoxicities on neonatal rat cardiomyocytes in vitro
AU - Qi, Zenghua
AU - Song, Yuanyuan
AU - Ding, Qianqian
AU - Liao, Xiaoliang
AU - Li, Ruijin
AU - Liu, Guoguang
AU - Tsang, Suk Ying
AU - CAI, Zongwei
N1 - Funding Information:
This study was supported by the Scientific Research Fund of Guangdong University of Technology (No. 220413595 ), the National Natural Science Foundation of China (No. 21806025 , 91543202 ), the General Research Fund ( 474913 ) from the University Grants Committee (UGC) of the Hong Kong SAR, and the Innovative Technology Fund of Innovation Technology Commission: Funding Support to Partner State Key Laboratories in Hong Kong, Collaborative Research Fund from Research Grant Council of Hong Kong (No. C2014-14E ).
Funding Information:
This study was supported by the Scientific Research Fund of Guangdong University of Technology (No. 220413595), the National Natural Science Foundation of China (No. 21806025, 91543202), the General Research Fund (474913) from the University Grants Committee (UGC) of the Hong Kong SAR, and the Innovative Technology Fund of Innovation Technology Commission: Funding Support to Partner State Key Laboratories in Hong Kong, Collaborative Research Fund from Research Grant Council of Hong Kong (No. C2014-14E).
PY - 2019/1/30
Y1 - 2019/1/30
N2 - A growing number of epidemiological surveys show that PM2.5 is an important promoter for the cardiovascular dysfunction induced by atmospheric pollution. PM2.5 is 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 PM2.5 fractions are still unclear, especially in the cellular level. Here we used the neonatal rat cardiomyocytes (NRCMs) to evaluate the cardiac toxicity of PM2.5 exposure. 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-PM2.5 or WIS-PM2.5 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-PM2.5 exposure could induce the cytotoxicity on NRCMs until the concentration of WS-PM2.5 was 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-PM2.5 or 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-PM2.5 and WIS-PM2.5 treatment group. In summary, our project not only estimates the risk of PM2.5 on cardiac cells but also reveal that Total-PM2.5 and WIS-PM2.5 exposure were predominantly associated with the functional cardiotoxicities in NRCMs.
AB - A growing number of epidemiological surveys show that PM2.5 is an important promoter for the cardiovascular dysfunction induced by atmospheric pollution. PM2.5 is 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 PM2.5 fractions are still unclear, especially in the cellular level. Here we used the neonatal rat cardiomyocytes (NRCMs) to evaluate the cardiac toxicity of PM2.5 exposure. 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-PM2.5 or WIS-PM2.5 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-PM2.5 exposure could induce the cytotoxicity on NRCMs until the concentration of WS-PM2.5 was 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-PM2.5 or 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-PM2.5 and WIS-PM2.5 treatment group. In summary, our project not only estimates the risk of PM2.5 on cardiac cells but also reveal that Total-PM2.5 and WIS-PM2.5 exposure were predominantly associated with the functional cardiotoxicities in NRCMs.
KW - Cardiac cell
KW - Cardiotoxicity
KW - Chemical composition
KW - Mitochondria
KW - PM
UR - http://www.scopus.com/inward/record.url?scp=85055916796&partnerID=8YFLogxK
U2 - 10.1016/j.ecoenv.2018.10.107
DO - 10.1016/j.ecoenv.2018.10.107
M3 - Journal article
C2 - 30396134
AN - SCOPUS:85055916796
SN - 0147-6513
VL - 168
SP - 378
EP - 387
JO - Ecotoxicology and Environmental Safety
JF - Ecotoxicology and Environmental Safety
ER -