Mitochondrial toxicity and in vitro biological effects of ambient PM2.5 from an urban site in China

Abstract The roles of PM2.5-induced mitochondrial damage and oxidative stress on mast cell degranulation were examined in vitro. Mast cells were treated with suspensions of PM2.5 in Dulbecco’s modified Eagle’s medium at concentrations from 25 to 200 mg/L in the absence or presence of 10 mmol/L N-acetyl-L-cysteine. Biological effects and mitochondrial function were assessed by determining cell viability, β-hexosaminidase release, interleukin-4 secretion, reactive oxygen species generation, adenosine triphosphate production, potential alteration of mitochondrial membrane, and activities of mitochondrial electron transport chain complexes I and III. Exposure of mast cells to PM2.5 induced reduction of adenosine triphosphate production, collapse of mitochondrial membrane potential, and inhibition of the activity of complex III. Co-treatment of mast cells exposed to PM2.5 with N-acetyl-L-cysteine attenuated cytotoxicity and the production of reactive oxygen species, and decreased the release of β-hexosaminidase and interleukin-4. Evidently, PM2.5-induced oxidative stress plays an essential role in mitochondrial toxicity and mast cell activation.