LAUSR

BACKGROUND Exposure to environmental chemicals has been linked with endothelial dysfunction, which is a leading cause of human diseases including atherosclerosis. Permethrin is a frequently used synthetic pyrethroid insecticide for which longer exposure may cause toxicities in several types of tissues and the development of metabolic diseases including atherosclerosis, obesity, and diabetes. The current study was designed to evaluate the potential adverse effect of permethrin on the function and activity of human endothelial cells. RESUTLS Permethrin was found to repress migration and tube formation by human umbilical vein endothelial cells (HUVECs) in a dose-dependent manner, and to significantly repress their viability after 24 and 48 h treatment. Furthermore, increased reactive oxygen species (ROS) production was observed in cells treated with permethrin, and the permethrin-induced repression of cell viability was ROS-dependent. Permethrin did not influence apoptosis, necrosis, or mitochondrial membrane potential in HUVECs. CONCLUSION The present results suggest that permethrin represses angiogenesis and viability through ROS-dependent and cell growth-, apoptosis- and necrosis-independent means. This article is protected by copyright. All rights reserved.