Oxidative stress and apoptosis are induced in human endothelial cells exposed to urban particulate matter

Correlations between exposure to particle matter (PM) with an aerodynamic diameter <= 2.5 or 10 Pm (PM2.5 and PM10, respectively) with cardiovascular effects have been demonstrated recently. Endothelial cells seem to play a relevant role in the responses to PM due to their participation in pro-inflammatory events. In this study we determined the effect of PM2.5 and PM10 from Mexico City on human endothelial cells by means of evaluating reactive oxygen species (ROS), nitric oxide (NO), NF-kappa B translocation and cell death. For this purpose we used human umbilical vein endothelial cells (HUVEC) as a model. The production of ROS was determined by the reduction of H(2)DCFDA and NO by Griess reagent. The translocation of NF-kappa B was evaluated by Electrophoretic Mobility Shift Assay (EMSA) and the cellular death by the translocation of phosphatidylserine. TNF-alpha was used as a positive control for endothelial cell activation. PM2.5 and PM10 induced the production of ROS (77% and 126% increase, respectively, vs. control) and NO (up to 132% and 233% increase, respectively, vs. control). PM2.5 and PM10 also induced the nuclear translocation of NF-kappa B. All these events were associated with apoptosis. In conclusion, the activation of HUVEC induced by PM2.5 and PM10 is related with an oxidative stress, suggesting that these particles may participate in the development of cardiovascular and inflammatory diseases. (C) 2009 Elsevier Ltd. All rights reserved.