| dc.description.abstract | Particulate matter (PM) such as ultrafine particulate matter (UFP) and the organic
compound pollutants such as polycyclic aromatic hydrocarbon (PAH) are widespread in the
environment. UFP and PAH are present in the air, and their presence may enhance their individual
adverse effects on human health. However, the mechanism and effect of their combined interactions
on human cells are not well understood. We investigated the combined toxicity of silica nanoparticles
(SiNPs) (UFP) and Benzo[a]pyrene (B[a]P) (PAH) on human endothelial cells. Human umbilical
vascular endothelial cells (HUVECs) were exposed to SiNPs or B[a]P, or a combination of SiNPs
and B[a]P. The toxicity was investigated by assessing cellular oxidative stress, DNA damage, cell
cycle arrest, and apoptosis. Our results show that SiNPs were able to induce reactive oxygen species
generation (ROS). B[a]P, when acting alone, had no toxicity effect. However, a co-exposure of SiNPs
and B[a]P synergistically induced DNA damage, oxidative stress, cell cycle arrest at the G2/M check
point, and apoptosis. The co-exposure induced G2/M arrest through the upregulation of Chk1
and downregulation of Cdc25C, cyclin B1. The co-exposure also upregulated bax, caspase-3, and
caspase-9, the proapoptic proteins, while down-regulating bcl-2, which is an antiapoptotic protein.
These results show that interactions between SiNPs and B[a]P synergistically potentiated toxicological
effects on HUVECs. This information should help further our understanding of the combined toxicity
of PAH and UFP. | en_US |
