PM2.5 and the typical components cause organelle damage, apoptosis and necrosis: Role of reactive oxygen species

Abstract

In this research, the organelle damage, apoptosis and necrosis induced by PM2.5, BC and Kaolin were studied using human bronchial epithelial (16HBE) cells. PM2.5, BC and Kaolin all induce cell death, LDH release and excess intracellular ROS generation. For the organelle injuries, Kaolin and high-dose PM2.5 (240 μg/mL) cause lysosomal acidification, but BC causes lysosomal alkalization (lysosomal membrane permeabilization, LMP). BC and Kaolin cause the loss of mitochondrial membrane potential (MMP), while PM2.5 does not. For the cell death mode, PM2.5 causes both apoptosis and necrosis. However only necrosis has been detected in the BC and Kaolin treated groups, indicating the more severe cellular insult. Excess ROS generation is involved in the organelle damage and cell death. ROS contributes to the BC-induced LMP and necrosis, but does not significantly affect the Kaolin-induced MMP loss and necrosis. Therefore, the BC component in PM2.5 may cause cytotoxicity via ROS-dependent pathways, the Kaolin component may damage cells via ROS-independent mechanisms such as strong interaction. The PM2.5-induced apoptosis and necrosis can be partially mitigated after the removal of ROS, indicating the existence of both the ROS-dependent and ROS-independent mechanisms due to the complicated PM2.5 components. BC represents the anthropogenic source component in PM2.5, while Kaolin represents the natural source component. Our results provide knowledge on the toxic mechanisms of typical PM2.5 components at the cellular and subcellular levels.