Fig. 2.

Exposure to PM caused mitochondrial oxidative stress and mitochondrial dysfunction in BEAS-2B cells. (A) Mitochondrial ROS production was increased dose-dependently. PM exposure increased the MitoSOX-detected red fluorescence intensity in BEAS-2B cells, but (B) pretreatment with NAC or MitoTEMPO (as mitochondria-targeted antioxidant) could significantly reduce the level of mitochondrial ROS. (C) Moreover, MitoTEMPO pretreatment also led to a decrease in intracellular ROS levels. Changes in (D, E) mitochondrial membrane potential (mtMP) determined as a red/green fluorescence ratio with JC-1 staining, (F) intracellular ATP levels and (G) mitochondrial DNA copy number (mtDNA-CN) were observed after PM exposure in the absence or presence of MitoTEMPO. Data are means ± SD of three independent experiments, and significant differences were expressed as followed: ^***P < 0.001 and ^**P < 0.01, compared with untreated cells (control); ^##P < 0.01 and ^#P < 0.05, compared with the PM-stimulated group