PMID- 29448021
OWN - NLM
STAT- MEDLINE
DCOM- 20181127
LR  - 20181127
IS  - 1879-1026 (Electronic)
IS  - 0048-9697 (Linking)
VI  - 628-629
DP  - 2018 Jul 1
TI  - Risk assessment of silica nanoparticles on liver injury in metabolic syndrome 
      mice induced by fructose.
PG  - 366-374
LID - S0048-9697(18)30431-5 [pii]
LID - 10.1016/j.scitotenv.2018.02.047 [doi]
AB  - This study aims to assess the effects and the mechanisms of silica nanoparticles 
      (SiNPs) on hepatotoxicity in both normal and metabolic syndrome mouse models 
      induced by fructose. Here, we found that SiNPs exposure lead to improved insulin 
      resistance in metabolic syndrome mice, but markedly worsened hepatic ballooning, 
      inflammation infiltration, and fibrosis. Moreover, SiNPs exposure aggravated 
      liver injury in metabolic syndrome mice by causing serious DNA damage. Following 
      SiNPs exposure, liver superoxide dismutase and catalase activities in metabolic 
      syndrome mice were stimulated, which is accompanied by significantly increased 
      malondialdehyde and 8-hydroxy-2-deoxyguanosine levels as compared to normal mice. 
      Scanning electron microscope (SEM) revealed that SiNPs were more readily 
      deposited in the liver mitochondria of metabolic syndrome mice, resulting in more 
      severe mitochondrial injury as compared to normal mice. We speculated that 
      SiNPs-induced mitochondrial injury might be the cause of hepatic oxidative 
      stress, which further lead to a series of liver lesions as observed in mice 
      following SiNPs exposure. Based on these results, it is likely that SiNPs will 
      increase the risk and severity of liver disease in individuals with metabolic 
      syndrome. Therefore, SiNPs should be used cautiously in food additives and 
      clinical settings.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Li, Jianmei
AU  - Li J
AD  - State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences 
      Nanjing University, Nanjing 210023, China.
FAU - He, Xiwei
AU  - He X
AD  - State Key Laboratory of Pollution Control and Resource Reuse, School of the 
      Environment, Nanjing University, Nanjing 210023, China.
FAU - Yang, Yang
AU  - Yang Y
AD  - State Key Laboratory of Pollution Control and Resource Reuse, School of the 
      Environment, Nanjing University, Nanjing 210023, China.
FAU - Li, Mei
AU  - Li M
AD  - State Key Laboratory of Pollution Control and Resource Reuse, School of the 
      Environment, Nanjing University, Nanjing 210023, China. Electronic address: 
      meili@nju.edu.cn.
FAU - Xu, Chenke
AU  - Xu C
AD  - State Key Laboratory of Pollution Control and Resource Reuse, School of the 
      Environment, Nanjing University, Nanjing 210023, China.
FAU - Yu, Rong
AU  - Yu R
AD  - State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences 
      Nanjing University, Nanjing 210023, China.
LA  - eng
PT  - Journal Article
DEP - 20180213
PL  - Netherlands
TA  - Sci Total Environ
JT  - The Science of the total environment
JID - 0330500
RN  - 30237-26-4 (Fructose)
RN  - 7631-86-9 (Silicon Dioxide)
SB  - IM
MH  - Animals
MH  - Fructose/*metabolism
MH  - Liver
MH  - Metabolic Syndrome/chemically induced/*metabolism
MH  - Mice
MH  - Nanoparticles/*toxicity
MH  - Oxidative Stress
MH  - Risk Assessment
MH  - Silicon Dioxide/*toxicity
OTO - NOTNLM
OT  - DNA damage
OT  - Hepatotoxicity
OT  - Metabolic syndrome
OT  - Oxidative stress
OT  - Silica nanoparticles
EDAT- 2018/02/16 06:00
MHDA- 2018/11/28 06:00
CRDT- 2018/02/16 06:00
PHST- 2017/12/09 00:00 [received]
PHST- 2018/01/30 00:00 [revised]
PHST- 2018/02/04 00:00 [accepted]
PHST- 2018/02/16 06:00 [pubmed]
PHST- 2018/11/28 06:00 [medline]
PHST- 2018/02/16 06:00 [entrez]
AID - S0048-9697(18)30431-5 [pii]
AID - 10.1016/j.scitotenv.2018.02.047 [doi]
PST - ppublish
SO  - Sci Total Environ. 2018 Jul 1;628-629:366-374. doi: 
      10.1016/j.scitotenv.2018.02.047. Epub 2018 Feb 13.