TY - JOUR
T1 - Fine particulate matter induces mitochondrial dysfunction and oxidative stress in human SH-SY5Y cells
AU - Wang, Ying
AU - Zhang, Mei
AU - Li, Zhiping
AU - Yue, Jianwei
AU - Xu, Min
AU - Zhang, Yanhao
AU - YUNG, Kin Lam
AU - Li, Ruijin
N1 - Funding Information:
This research was supported by the National Natural Science Foundation of China (No. 91543202 ) and the Hundred Talents Program of Shanxi Province in China .
PY - 2019/3
Y1 - 2019/3
N2 - 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.
AB - 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.
KW - Fine particulate matter
KW - Human SH-SY5Y cells
KW - Mitochondrial dysfunction
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=85059301356&partnerID=8YFLogxK
U2 - 10.1016/j.chemosphere.2018.11.149
DO - 10.1016/j.chemosphere.2018.11.149
M3 - Article
C2 - 30502696
AN - SCOPUS:85059301356
SN - 0045-6535
VL - 218
SP - 577
EP - 588
JO - Chemosphere
JF - Chemosphere
ER -
