Oxidative stress induced by urban fine particles in cultured EA.hy926 cells.

It has been reported that vascular endothelia cell damage is an important precursor to the morbidity and mortality associated with cardiovascular disease exposed to airborne particulate matter (PM). The present study investigated the hypothesis that urban fine (PM(2.5)) particles could cause cytotoxicity via oxidative stress in human umbilical vein endothelial cells, EA.hy926. The concentrations of metal elements (Cr, Fe, Ni, Cu, Zn, Mo, Cd and Pb) in PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) were determined by inductively coupled plasma - mass spectrometry (ICP-MS). Iron (Fe), Zn and Pb were highly enriched in all the samples. Exposure of the cultured EA.hy926 cells to PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) led to cell death, reactive oxygen species (ROS) increase, mitochondrial transmembrane potential (ΔΨm) disruption and NF-κB activation, respectively. The ROS increase by exposure to PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) triggered the activation of nuclear factor (NF)-κB, which means that PM(2.5) particles exert cytotoxicity by an apopotic process. However, the induction of cytotoxicity by PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) was reversed by pretreatment with superoxide dismutase (SOD). These results suggest that each fraction of PM(2.5) has a potency to cause oxidative stress in endothelial cells. ROS was generated through PM(2.5)-mediated mitochondrial apoptotic pathway, which may induce direct interaction between metal elements and endothelia cells.