Tetrachlorobisphenol A Induces Programmed Cell Death and Senescence in Vascular Endothelial Cells

Abstract

Tetrachlorobisphenol A (TCBPA) is an organic compound extensively utilized in industrial production as an alternative to Tetrabromobisphenol A (TBBPA). Currently, TCBPA has been frequently detected in various environmental media. TCBPA residues have been detected in environmental samples, prompting concerns about its potential toxicological impact on human health. This study focuses on the potential impact of TCBPA on vascular health, particularly its effects on vascular endothelial cells. Through CCK8 and EdU assays, we observed that TCBPA treatment inhibited the proliferation of vascular endothelial cells. Further studies showed that TCBPA triggers an inflammatory response in vascular endothelial cells, including IL-6, IL-1β, and TNF-α. Additionally, TCBPA was found to trigger oxidative stress in vascular endothelial cells, as evidenced by increased levels of reactive oxygen species (ROS). Further studies demonstrated that TCBPA led to programmed necrosis and senescence in vascular endothelial cells. Mechanistically, we discovered that ROS-induced mitochondrial Z-DNA played a critical role in this process. Our findings suggest that TCBPA may inhibit vascular endothelial cell proliferation, posing a potential risk for vascular damage. This study highlights the importance of regulating TCBPA usage to minimize potential health risks.