摘要
Objective To explore the relationship between different components of fine particulate matter（PM2.5） emitted from coal combustion and their cytotoxic effect in the vascular endothelial cells. Methods Coal-fired PM2.5 was sampled using a fixed-source dilution channel and flow sampler. The sample components were analyzed by ion chromatography and inductively coupled plasma atomic emission spectroscopy（ICP-AES）. The PM2.5 suspension was extracted using an ultrasonic water-bath method and then human umbilical vein endothelial cells（EA.hy926） were treated with various concentrations of the PM2.5 suspension. Cell proliferation, oxidative DNA damage, and global DNA methylation levels were used to measure the cellular toxicity of PM2.5 emitted from coal combustion. Results Compared to other types of coal-fired PM2.5 preparations, the PM2.5 suspension from Yinchuan coal had the highest cytotoxicity. PM2.5 suspension from Datong coal had the highest toxic effect while that from Yinchuan coal had the lowest. Exposure to coal-fired PM2.5 from Jingxi coal resulted in lower 8-hydroxy-2’-deoxyguanosine（8-OHd G） levels. At the same dose, PM2.5 emitted from coal combustion could produce more severe DNA impairment compared to that produced by carbon black. Cell survival rate was negatively correlated with chloride and potassium ions content. The 5-methylcytosine（5-m C） level was positively correlated with Mn and negatively correlated with Zn levels. The 8-OHd G% level was positively correlated with both Mn and Fe. Conclusion PM2.5 emitted from coal combustion can decrease cell viability, increase global DNA methylation, and cause oxidative DNA damage in EA.hy926 cells. Metal components may be important factors that influence cellular toxicity.
Objective To explore the relationship between different components of fine particulate matter（PM2.5） emitted from coal combustion and their cytotoxic effect in the vascular endothelial cells. Methods Coal-fired PM2.5 was sampled using a fixed-source dilution channel and flow sampler. The sample components were analyzed by ion chromatography and inductively coupled plasma atomic emission spectroscopy（ICP-AES）. The PM2.5 suspension was extracted using an ultrasonic water-bath method and then human umbilical vein endothelial cells（EA.hy926） were treated with various concentrations of the PM2.5 suspension. Cell proliferation, oxidative DNA damage, and global DNA methylation levels were used to measure the cellular toxicity of PM2.5 emitted from coal combustion. Results Compared to other types of coal-fired PM2.5 preparations, the PM2.5 suspension from Yinchuan coal had the highest cytotoxicity. PM2.5 suspension from Datong coal had the highest toxic effect while that from Yinchuan coal had the lowest. Exposure to coal-fired PM2.5 from Jingxi coal resulted in lower 8-hydroxy-2’-deoxyguanosine（8-OHd G） levels. At the same dose, PM2.5 emitted from coal combustion could produce more severe DNA impairment compared to that produced by carbon black. Cell survival rate was negatively correlated with chloride and potassium ions content. The 5-methylcytosine（5-m C） level was positively correlated with Mn and negatively correlated with Zn levels. The 8-OHd G% level was positively correlated with both Mn and Fe. Conclusion PM2.5 emitted from coal combustion can decrease cell viability, increase global DNA methylation, and cause oxidative DNA damage in EA.hy926 cells. Metal components may be important factors that influence cellular toxicity.
基金
supported by the National Science Foundation for Distinguished Young Scholars of China(Grant No.21507122)
