Airborne nanoparticles (PM0.1) induce autophagic cell death of human neuronal cells.

Airborne nanoparticles PM_0.1 (<100 nm in diameter) were collected and their chemical composition was determined. Al was by far the most abundant metal in the PM_0.1 followed by Zn, Cr, Mn, Cu, Pb and Ni. Exposure to PM_0.1 resulted in a cell viability decrease in human neuronal cells SH-SY5Y in a concentration-dependent manner. Upon treatment with N-acetylcysteine, however, cell viability was significantly recovered, suggesting the involvement of reactive oxygen species (ROS). Cellular DNA damage by PM_0.1 was also detected by the Comet assay. PM_0.1-induced autophagic cell death was explained by an increase in the expression of microtubule-associated protein light chain 3A-ІІ (LC3A-ІІ) and autophagy-related protein Atg 3 and Atg 7. Analysis of 2-DE gels revealed that six proteins were upregulated, whereas eight proteins were downregulated by PM_0.1 exposure. Neuroinflammation-related lithostathine and cyclophilin A complexed with dipeptide Gly-Pro, autophagy-related heat shock protein gp96 and neurodegeneration-related triosephosphate isomerase were significantly changed upon exposure to PM_0.1. These results, taken together, suggest that PM_0.1-induced oxidative stress via ROS generation plays a key role in autophagic cell death and differential protein expressions in SH-SY5Y cells. This might provide a plausible explanation for the underlying mechanisms of PM_0.1 toxicity in neuronal cells and even the pathogenesis of diseases associated with its exposure. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]