PMID- 17374408
OWN - NLM
STAT- MEDLINE
DCOM- 20070817
LR  - 20161124
IS  - 0166-445X (Print)
IS  - 0166-445X (Linking)
VI  - 82
IP  - 2
DP  - 2007 May 1
TI  - Induction of oxidative stress and apoptosis by PFOS and PFOA in primary cultured 
      hepatocytes of freshwater tilapia (Oreochromis niloticus).
PG  - 135-43
AB  - Perfluorinated organic compounds (PFOCs) are emerging persistent organic 
      pollutants (POPs) widely present in the environment, wildlife and human. We 
      studied the cellular toxicology of perfluorooctane sulfonate (PFOS) and 
      perfluorooctanoic acid (PFOA) on oxidative stress and induction of apoptosis in 
      primary cultured hepatocytes of freshwater tilapia (Oreochromis niloticus). 
      Cultured hepatocytes were exposed to PFOS or PFOA (0, 1, 5, 15 and 30 mg L(-1)) 
      for 24h, and a dose-dependent decrease in cell viability was determined using 
      trypan blue exclusion method. Significant induction of reactive oxygen species 
      (ROS) accompanied by increases in activities of superoxide dismutase (SOD), 
      catalase (CAT) and glutathione reductase (GR) were found, while activities of 
      glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were decreased. 
      Glutathione (GSH) content was reduced following treatment of PFOA and PFOS. A 
      dose-dependent increase in the lipid peroxidation (LPO) level (measured as maleic 
      dialdehyde, MDA) was observed only in the PFOA exposure groups, whereas LPO 
      remained unchanged in the PFOS exposure groups. Furthermore, a significant 
      activation of caspase-3, -8, -9 activities was evident in both PFOS and PFOA 
      exposure groups. Typical DNA fragmentation (DNA laddering) was further 
      characterized by agarose gel electrophoresis. The overall results demonstrated 
      that PFOS and PFOA are able to produce oxidative stress and induce apoptosis with 
      involvement of caspases in primary cultured tilapia hepatocytes.
FAU - Liu, Chunsheng
AU  - Liu C
AD  - State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of 
      Hydrobiology, The Chinese Academy of Sciences, Wuhan 430072, PR China.
FAU - Yu, Ke
AU  - Yu K
FAU - Shi, Xiongjie
AU  - Shi X
FAU - Wang, Jingxian
AU  - Wang J
FAU - Lam, Paul K S
AU  - Lam PK
FAU - Wu, Rudolf S S
AU  - Wu RS
FAU - Zhou, Bingsheng
AU  - Zhou B
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070215
PL  - Netherlands
TA  - Aquat Toxicol
JT  - Aquatic toxicology (Amsterdam, Netherlands)
JID - 8500246
RN  - 0 (Alkanesulfonic Acids)
RN  - 0 (Caprylates)
RN  - 0 (Enzymes)
RN  - 0 (Fluorocarbons)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Water Pollutants, Chemical)
RN  - 947VD76D3L (perfluorooctanoic acid)
RN  - 9H2MAI21CL (perfluorooctane sulfonic acid)
RN  - EC 3.4.22.- (Caspases)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Alkanesulfonic Acids/*toxicity
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Caprylates/*toxicity
MH  - Caspases/analysis/drug effects/metabolism
MH  - Cichlids/*physiology
MH  - DNA Fragmentation/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Enzymes/analysis/drug effects
MH  - Fluorocarbons/*toxicity
MH  - Fresh Water
MH  - Glutathione/analysis
MH  - Hepatocytes/cytology/*drug effects
MH  - Lipid Peroxidation/drug effects
MH  - Oxidative Stress/drug effects
MH  - Reactive Oxygen Species/analysis
MH  - Water Pollutants, Chemical/*toxicity
EDAT- 2007/03/22 09:00
MHDA- 2007/08/19 09:00
CRDT- 2007/03/22 09:00
PHST- 2006/12/04 00:00 [received]
PHST- 2007/02/06 00:00 [revised]
PHST- 2007/02/08 00:00 [accepted]
PHST- 2007/03/22 09:00 [pubmed]
PHST- 2007/08/19 09:00 [medline]
PHST- 2007/03/22 09:00 [entrez]
AID - S0166-445X(07)00060-4 [pii]
AID - 10.1016/j.aquatox.2007.02.006 [doi]
PST - ppublish
SO  - Aquat Toxicol. 2007 May 1;82(2):135-43. doi: 10.1016/j.aquatox.2007.02.006. Epub 
      2007 Feb 15.