PMID- 23618922
OWN - NLM
STAT- MEDLINE
DCOM- 20130723
LR  - 20161125
IS  - 0027-5107 (Print)
IS  - 0027-5107 (Linking)
VI  - 754
IP  - 1-2
DP  - 2013 Jun 14
TI  - PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster 
      hybrid cells.
PG  - 51-7
LID - S1383-5718(13)00094-6 [pii]
LID - 10.1016/j.mrgentox.2013.04.004 [doi]
AB  - Perfluorooctane sulfonate (PFOS) was listed as one of the persistent organic 
      pollutants (POPs) in Stockholm Convention in 2009. Recent evidence showed that 
      PFOS could induce apoptosis both in vivo and in vitro. However, the apoptotic 
      mechanisms induced by PFOS as well as the possible relationship between apoptosis 
      and other PFOS-induced endpoints, remain unclear. In the present study, normal 
      human-hamster hybrid (AL) cells and mtDNA-depleted (rho(0) AL) cells were exposed 
      to PFOS, and assayed for cytotoxicity, mutagenicity, and apoptosis (caspase-3/7, 
      caspase-9 activities). Our results showed that PFOS decreased cell viability in a 
      time- and concentration-dependent manner in AL cells, but not in rho(0) AL cells. 
      However, long-term exposure to PFOS failed to induce the mutagenic effects at the 
      CD59 locus in AL cells. Exposure to 200 muM PFOS significantly increased the 
      activities of caspase-3/7 and caspase-9 in AL cells, but the activities of these 
      caspases were not affected in rho(0) AL cells. In addition, PFOS increased the 
      levels of reactive oxygen species (ROS), superoxide anion (O2(-)), as well as 
      nitric oxide (NO), and decreased mitochondrial membrane potential (MMP) at the 
      concentrations of 100 and 200muM in AL cells. On the other hand, exposure to PFOS 
      had no effect on intracellular ROS, O2(-), and NO production in rho(0) AL cells. 
      Caspase-3/7 activity, which was increased by 200 muM PFOS, could be suppressed by 
      ROS/O2(-) scavengers and nitric oxide synthases (NOSs) inhibitors in AL cells. 
      These results implicate that PFOS-induced apoptosis and oxidative stress is 
      mediated by a mitochondrion-dependent pathway and that the induction of apoptosis 
      might be a protective function against mutagenesis in AL cells exposed to PFOS.
CI  - Copyright (c) 2013 Elsevier B.V. All rights reserved.
FAU - Wang, Xiaofei
AU  - Wang X
AD  - Key Laboratory of Ion Beam Bioengineering, Hefei Institutes of Physical Science, 
      Chinese Academy of Sciences, Hefei, Anhui, PR China.
FAU - Zhao, Guoping
AU  - Zhao G
FAU - Liang, Junting
AU  - Liang J
FAU - Jiang, Jiang
AU  - Jiang J
FAU - Chen, Ni
AU  - Chen N
FAU - Yu, Jing
AU  - Yu J
FAU - Wang, Qisen
AU  - Wang Q
FAU - Xu, An
AU  - Xu A
FAU - Chen, Shaopeng
AU  - Chen S
FAU - Wu, Lijun
AU  - Wu L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130422
PL  - Netherlands
TA  - Mutat Res
JT  - Mutation research
JID - 0400763
RN  - 0 (Alkanesulfonic Acids)
RN  - 0 (Fluorocarbons)
RN  - 0 (Free Radical Scavengers)
RN  - 0 (Mutagens)
RN  - 0 (Reactive Oxygen Species)
RN  - 11062-77-4 (Superoxides)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 9H2MAI21CL (perfluorooctane sulfonic acid)
SB  - IM
MH  - Alkanesulfonic Acids/*toxicity
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cell Line
MH  - Cricetinae
MH  - Fluorocarbons/*toxicity
MH  - Free Radical Scavengers/pharmacology
MH  - Humans
MH  - *Hybrid Cells
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mitochondria/*drug effects/metabolism
MH  - Mutagens/*toxicity
MH  - Nitric Oxide/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Superoxides/metabolism
EDAT- 2013/04/27 06:00
MHDA- 2013/07/24 06:00
CRDT- 2013/04/27 06:00
PHST- 2012/09/21 00:00 [received]
PHST- 2013/04/05 00:00 [revised]
PHST- 2013/04/16 00:00 [accepted]
PHST- 2013/04/27 06:00 [entrez]
PHST- 2013/04/27 06:00 [pubmed]
PHST- 2013/07/24 06:00 [medline]
AID - S1383-5718(13)00094-6 [pii]
AID - 10.1016/j.mrgentox.2013.04.004 [doi]
PST - ppublish
SO  - Mutat Res. 2013 Jun 14;754(1-2):51-7. doi: 10.1016/j.mrgentox.2013.04.004. Epub 
      2013 Apr 22.