Mitochondrial damage mediated by ROS incurs bronchial epithelial cell apoptosis upon ambient PM<sub>2.5</sub> exposure

Abstract

Mitochondria can be used as important biomarkers of pollutants on human health, and fine particulate matter (PM_2.5) has been documented to cause respiratory damage. However, current studies about the relationship between PM_2.5 and mitochondria in respiratory tract are limited and warrant further detailed investigations. Hence, the study was aimed to evaluate effects of PM_2.5 on mitochondrial structure, investigate the link between PM_2.5-induced mitochondrial disorder and respiratory damage, and delineate the possible mechanisms using both in vitro and in vivo models. PM_2.5 exposure resulted in damage of mitochondrial structure, including mitochondrial dynamic, DNA biogenesis and morphological alteration 16HBE cells. Furthermore, PM_2.5 elevated ROS formation. However, DPI and NAC (inhibitor of ROS) in supplement restored PM_2.5-induced mitochondrial disorder. PM_2.5 also contributed to the 16HBE cells apoptosis via mitochondrial pathway. Additionally, the results coincided with the in vivo data which were obtained from bronchial tissues of SD rats exposed to PM_2.5 for 30 days. Collectively, this study uncovers that PM_2.5 leads to the disorder of mitochondrial structure via ROS generation, and then results in respiratory damage. It provides further understanding about the detrimental effect of PM_2.5 on respiratory damage, and reveals a mechanistic basis for preventing outcomes in polluted environments.