Abstract
BACKGROUND/AIM: Arsenic trioxide (As(2)O(3)) is an environmental pollutant. However, the detailed mechanisms about As(2)O(3)-induced loss of endothelial integrity are unknown. This study aimed at investigating how As(2)O(3) causes endothelial dysfunction and whether baicalin can reverse such dysfunction. MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were used to examine As(2)O(3)-induced oxidative stress, and apoptosis. The influence of baicalin on As(2)O(3)-induced endothelial dysfunction were investigated. RESULTS: The viability of HUVECs was inhibited by As(2)O(3) and cells underwent apoptosis. As(2)O(3) treatment increased NADPH oxidase activity, and elevated the level of reactive oxygen species (ROS). Formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were accumulated. Baicalin reversed As(2)O(3)-induced apoptosis and As(2)O(3)-suppressed cell viability. Baicalin caused a decrease in NADPH oxidase activity, and re-balanced the ROS level. As(2)O(3)-induced formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were down-regulated. CONCLUSION: Baicalin was found to have the potential capacity to protect endothelial cells from As(2)O(3)-induced cytotoxicity.