Airborne Quinones Caused Cytotoxicity and DNA Damage in Human Vascular Endothelial Cells

Abstract

Traffic-related particulate matter (PM) is found to be associated with adverse cardiovascular diseases. Quinones present in the traffic-related PM are hypothesized to contribute to these harmful effects through reactive oxygen species (ROS) generation. However, the impacts of the airborne quinones on the cytotoxic and genotoxic effects in human vascular endothelial cells are less well known. The aim of the present study is to assess whether exposure to three typical airborne quinones, including anthraquinone (AQ), 1,4-naphthroquinone (NQ) and benzoquinone (BQ), can induce cytotoxicity and DNA damage in the human umbilical vein endothelial cells (HUVEC). Cell viability, plasma membrane damage (lactate dehydrogenase leakage), and DNA damage were assessed in HUVEC after exposed to the three airborne quinones. Significant cytotoxicity was caused by the three quinones, indicating by the significant decrease in cell viability and significant increase in LDH activity. AQ and BQ slightly increased the DNA damage in HUVEC without significance. The ROS generation was not observed in HUVEC after exposed to AQ, NQ or BQ, suggesting that the cyototoxicity and the DNA damage caused by these quinones in HUVEC were not generated through the oxidative stress pathway. Our results suggest that AQ, NQ and BQ presented in the traffic-related particles may participate in the development of cardiovascular diseases through causing cytotoxicity and DNA damage in vascular endothelial cells.