Mitochondrial toxicity and <i>in vitro</i> biological effects of ambient PM_2.5 from an urban site in China

The roles of PM_2.5-induced mitochondrial damage and oxidative stress on mast cell degranulation were examined <i>in vitro</i>. Mast cells were treated with suspensions of PM_2.5 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 PM_2.5 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 PM_2.5 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, PM_2.5-induced oxidative stress plays an essential role in mitochondrial toxicity and mast cell activation.