Co-exposure to polystyrene nanoplastics and F-53B induces vascular endothelial cell pyroptosis through the NF-κB/NLRP3 pathway

Abstract

6:2 Chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA; trade name F-53B) is an alternative to perfluorooctane sulfonate (PFOS) and is widely detected in various environmental media and biological samples. Polystyrene nanoplastics (PS-NPs) have become a significant pollutant in the global environment. However, the comprehensive effects of both on the vascular system of mammals are still unclear. This study aims to explore the impacts of F-53B and PS-NPs exposure on the vascular system. Experimental findings indicate that both individual and co-exposure to F-53B and PS-NPs could lead to arterial wall thickening, increase collagen deposition, and reduce elasticity in mice. Moreover, co-exposure results in loss of endothelial integrity, impairs the repair capabilities of endothelial cells by inhibiting their proliferation and migration, and increases the levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Mechanistic studies reveal that F-53B and PS-NPs exposure activate the NF-κB/NLRP3 signaling pathway, promoting endothelial cell pyroptosis and ultimately inducing vascular damage. In summary, this study provides novel insights into the synergistic impact of F-53B and PS-NPs on vascular injury, shedding light on the mechanism underlying the combined toxicity of PS-NPs and other pollutants.

Keywords: Co-exposure; Endothelial cells; F-53B; Polystyrene nanoplastics; Pyroptosis.