Abstract: Exposure to fine ambient particulate matter (PM_2.5) is known to be associated with cardiovascular disease. To uncover the molecular mechanisms involved in cardiovascular toxicity of PM_2.5, we investigated alterations in the protein profile of human umbilical vein endothelial cells (HUVECs) treated with PM_2.5 using two-dimensional electrophoresis in conjunction with mass spectrometry (MS). A total of 31 protein spots were selected as differentially expressed proteins and identified by matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) MS. The results demonstrated that DNA damage and cell apoptosis are important factors contributing to PM_2.5-mediated toxicity in HUVECs. It is further proposed that PM_2.5 can inhibit superoxide dismutase (SOD) activity and increase reactive oxygen species (ROS) and malonaldehyde (MDA) production in a concentration-dependent manner. Induction of apoptosis and DNA damage through oxidative stress pathways may be one of the key toxicological events occurring in HUVECs under PM_2.5 stress. These results indicated that the toxic mechanisms of PM_2.5 on cardiovascular disease are related to endothelial dysfunction.

Key words: Fine ambient particulate matter (PM_2.5); Human umbilical vein endothelial cell (HUVEC); Proteomics; Toxic mechanism

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