PMID- 24583672
OWN - NLM
STAT- MEDLINE
DCOM- 20141113
LR  - 20140324
IS  - 1873-3336 (Electronic)
IS  - 0304-3894 (Linking)
VI  - 270
DP  - 2014 Apr 15
TI  - Silica nanoparticles induce autophagy and autophagic cell death in HepG2 cells 
      triggered by reactive oxygen species.
PG  - 176-86
LID - S0304-3894(14)00042-9 [pii]
LID - 10.1016/j.jhazmat.2014.01.028 [doi]
AB  - Silica nanoparticles (SNPs) are becoming favorable carriers for drug delivery or 
      gene therapy, and in turn, the toxic effect of SNPs on biological systems is 
      gaining attention. Currently, autophagy is recognized as an emerging toxicity 
      mechanism triggered by nanomaterials, yet there have been scarcely research about 
      the mechanisms of autophagy and autophagic cell death associated with SNPs. In 
      this study, we verified the activation of SNPs-induced autophagy via the 
      MDC-staining and LC3-I/LC3-II conversion, resulted in a dose-dependent manner. 
      The typically morphological characteristics (autophagosomes and autolysosomes) of 
      the autophagy process were observed in TEM ultrastructural analysis. In addition, 
      the autophagic cell death was evaluated by cellular co-staining assay. And the 
      underlying mechanisms of autophagy and autophagic cell death were performed using 
      the intracellular ROS detection, autophagy inhibitor and ROS scavenger. Results 
      showed that the elevated ROS level was in line with the increasing of autophagy 
      activation, while both the 3-MA and NAC inhibitors effectively suppressed the 
      autophagy and cell death induced by SNPs. In summary, our findings demonstrated 
      that the SNPs-induced autophagy and autophagic cell death were triggered by the 
      ROS generation in HepG2 cells, suggesting that exposure to SNPs could be a 
      potential hazardous factor for maintaining cellular homeostasis.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Yu, Yongbo
AU  - Yu Y
AD  - School of Public Health, Capital Medical University, Beijing, 100069, P.R. China; 
      Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, 100069, P.R. China.
FAU - Duan, Junchao
AU  - Duan J
AD  - School of Public Health, Capital Medical University, Beijing, 100069, P.R. China; 
      Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, 100069, P.R. China.
FAU - Yu, Yang
AU  - Yu Y
AD  - School of Public Health, Capital Medical University, Beijing, 100069, P.R. China; 
      Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, 100069, P.R. China.
FAU - Li, Yang
AU  - Li Y
AD  - School of Public Health, Capital Medical University, Beijing, 100069, P.R. China; 
      Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, 100069, P.R. China.
FAU - Liu, Xiaomei
AU  - Liu X
AD  - School of Public Health, Jilin University, Changchun, Jilin, 130021, P.R. China.
FAU - Zhou, Xianqing
AU  - Zhou X
AD  - School of Public Health, Capital Medical University, Beijing, 100069, P.R. China; 
      Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, 100069, P.R. China.
FAU - Ho, Kin-Fai
AU  - Ho KF
AD  - School of Public Health and Primary Care, Chinese University of Hong Kong, Hong 
      Kong, China.
FAU - Tian, Linwei
AU  - Tian L
AD  - School of Public Health and Primary Care, Chinese University of Hong Kong, Hong 
      Kong, China. Electronic address: linweit@cuhk.edu.hk.
FAU - Sun, Zhiwei
AU  - Sun Z
AD  - School of Public Health, Capital Medical University, Beijing, 100069, P.R. China; 
      Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, 100069, P.R. China. Electronic address: zwsun@hotmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140124
PL  - Netherlands
TA  - J Hazard Mater
JT  - Journal of hazardous materials
JID - 9422688
RN  - 0 (Reactive Oxygen Species)
RN  - 7631-86-9 (Silicon Dioxide)
SB  - IM
MH  - Autophagy/drug effects
MH  - Cell Survival/drug effects
MH  - Hep G2 Cells
MH  - Humans
MH  - Microscopy, Electron, Transmission
MH  - Nanoparticles/*toxicity/ultrastructure
MH  - Reactive Oxygen Species/*metabolism
MH  - Silicon Dioxide/*toxicity
OTO - NOTNLM
OT  - Autophagic cell death
OT  - Autophagy
OT  - Nanotoxicity
OT  - Reactive oxygen species
OT  - Silica nanoparticles
EDAT- 2014/03/04 06:00
MHDA- 2014/11/14 06:00
CRDT- 2014/03/04 06:00
PHST- 2013/09/30 00:00 [received]
PHST- 2013/12/22 00:00 [revised]
PHST- 2014/01/07 00:00 [accepted]
PHST- 2014/03/04 06:00 [entrez]
PHST- 2014/03/04 06:00 [pubmed]
PHST- 2014/11/14 06:00 [medline]
AID - S0304-3894(14)00042-9 [pii]
AID - 10.1016/j.jhazmat.2014.01.028 [doi]
PST - ppublish
SO  - J Hazard Mater. 2014 Apr 15;270:176-86. doi: 10.1016/j.jhazmat.2014.01.028. Epub 
      2014 Jan 24.