AIM:To study the toxicity of PM2.5 in the endothelial cells by investigating the induction of reactive oxygen species (ROS) and apoptosis in EA.hy926 cells exposed to PM2.5.METHODS: The endothelial cell line EA. hy926 was cultured in vitro and exposed to PM2.5 at different concentrations for 24 h.The cell viability was measured by CCK-8 assay and the generation of intracellular ROS was stained with DCFH-DA.The cell apoptosis was analyzed by flow cy-tometry with Annexin V-FITC/PI staining, and the protein levels of cytochrome C , caspase 9 and caspase 3 was detected by Western blot.RESULTS:After the treatment with PM2.5, the viability of the EA.hy926 cells was decreased markedly and the production of ROS was increased significantly .PM2.5 exposure upregulated the expression of cytoplasm cytochrome C and activated caspase-9 and caspase-3, resulting in the increase of the cell apoptosis significantly .The ROS generation was direct-ly involved in PM2.5-mediated endothelial cell apoptosis as N-acetyl-L-cysteine pretreatment abolished both ROS production and cell apoptosis induced by PM 2.5.CONCLUSION:PM2.5 induces oxidative stress and apoptosis in the vascular endo-thelial cells, which may be one of the mechanisms that PM2.5 influences the function of cardiovascular system .