Fine particulate matter induces mitochondrial dysfunction and oxidative stress in human SH-SY5Y cells

Ying Wang, Mei Zhang, Zhiping Li, Jianwei Yue, Min Xu, Yanhao Zhang, Ken Kin Lam Yung*, Ruijin Li*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

93 Citations (Scopus)


Exposure to ambient fine particulate matter (PM2.5) is associated with neurodegenerative diseases. Mitochondrion is key to brain degeneration. However, the underlying mechanism of PM2.5-induced brain injury, especially mitochondrial damage, is still unclear. In this study, changes in mitochondrial dynamics, mitochondrial permeability transition pore (mPTP), mitochondrial DNA (mtDNA) and oxidative stress in human SH-SY5Y cells exposed to PM2.5 at different concentrations (0, 25, 100, and 250 μg mL−1) were investigated. The results showed that PM2.5 caused more mitochondrial swell, accompanied by the opening of mPTP and the decrease of ATP levels, mitochondrial membrane potential and mtDNA copy number in SH-SY5Y cells. PM2.5 significantly enhanced the expression of mitochondrial fission/fusion genes (Drp1 and OPA1) and affected the gene expression of CypD, SIRT3, and COX Ⅳ in SH-SY5Y cells. Besides, PM2.5 triggered the increase of cellular ROS, Ca2+ and Aβ-42 levels, inhibition of manganese-superoxide dismutase (SOD2) activities, reduction of GSH levels GSH/GSSG ratio, and elevation of mitochondrial malondialdehyde contents. It suggests that mitochondrial dysfunction and oxidative stress are the potential mechanisms underlying PM2.5-induced brain nerve cell injury, which may be related to neurological diseases. Additionally, our study elucidated that PM2.5 components trigger different cytotoxicity.

Original languageEnglish
Pages (from-to)577-588
Number of pages12
Early online date23 Nov 2018
Publication statusPublished - Mar 2019

Scopus Subject Areas

  • Environmental Engineering
  • Environmental Chemistry
  • Chemistry(all)
  • Pollution
  • Health, Toxicology and Mutagenesis

User-Defined Keywords

  • Fine particulate matter
  • Human SH-SY5Y cells
  • Mitochondrial dysfunction
  • Oxidative stress


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