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

Authors
Jeon, Yu-MiLee, Mi-Young
Issue Date
Oct-2016
Publisher
WILEY
Keywords
airborne nanoparticles (PM0.1); SH-SY5Y cells; reactive oxygen species; autophagic cell death; proteomics
Citation
JOURNAL OF APPLIED TOXICOLOGY, v.36, no.10, pp.1332 - 1342
Journal Title
JOURNAL OF APPLIED TOXICOLOGY
Volume
36
Number
10
Start Page
1332
End Page
1342
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/850
DOI
10.1002/jat.3324
ISSN
0260-437X
Abstract
Airborne nanoparticles PM0.1 (<100nm in diameter) were collected and their chemical composition was determined. Al was by far the most abundant metal in the PM0.1 followed by Zn, Cr, Mn, Cu, Pb and Ni. Exposure to PM0.1 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 PM0.1 was also detected by the Comet assay. PM0.1-induced autophagic cell death was explained by an increase in the expression of microtubule-associated protein light chain 3A- (LC3A-) 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 PM0.1 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 PM0.1. These results, taken together, suggest that PM0.1-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 PM0.1 toxicity in neuronal cells and even the pathogenesis of diseases associated with its exposure. Copyright (c) 2016 John Wiley & Sons, Ltd.
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