PMID- 19041924
OWN - NLM
STAT- MEDLINE
DCOM- 20090324
LR  - 20161124
IS  - 0300-483X (Print)
IS  - 0300-483X (Linking)
VI  - 256
IP  - 1-2
DP  - 2009 Feb 4
TI  - Cleft palate caused by perfluorooctane sulfonate is caused mainly by extrinsic 
      factors.
PG  - 42-7
LID - 10.1016/j.tox.2008.11.003 [doi]
AB  - Perfluorooctane sulfonate (PFOS) is found ubiquitously in the environment, and is 
      known to cause developmental toxicity, including cleft plate (CP). The aim of the 
      present study was to elucidate the mechanism of CP associated with in utero 
      exposure to PFOS in mice. We first examined whether the concentration of PFOS in 
      fetal serum was related to susceptibility to CP. We compared palatogenesis 
      following the administration of various concentrations of PFOS to dams. We 
      conducted histological examination on gestational day (GD) 15 and 18, and 
      alizarin red/alcian blue staining of fetal heads on GD18. Finally, we cultured 
      palatal shelves (PSs) of GD14 fetuses, which had not yet made contact with each 
      other, for 48h, to examine whether the shelves maintained the ability to fuse. 
      The incidence of CP increased from 7.3% with a fetal serum concentration of PFOS 
      of 110.7+/-13.4microg/ml (13mg/kg) to 78.3% with 138.6+/-0.9microg/ml (20mg/kg). 
      PFOS at 50mg/kg on GD11-15 caused CP at a rate of 6.1%, meanwhile PFOS at 20mg/kg 
      on GD1-17 caused a CP rate of 89.3%. Failure of palatal shelf elevation was 
      observed with 20mg/kg PFOS. PFOS at 20mg/kg on GD1-17 and 50mg/kg on GD11-15 
      inhibited mandibular growth to the same extent, even though the rate of CP was 
      different. Explants exposed to PFOS 20mg/kg and Tween 20 showed 94% (34/36) and 
      100% (31/31) fusion, respectively. We demonstrated that increasing the oral dose 
      of PFOS from 13 to 20mg/kg resulted in a significant increase in CP even though 
      there was only a small increase in serum concentration of PFOS. PFOS prevented 
      elevation of the PSs above the tongue because their growth/fusion potential was 
      maintained. Mandibular hypoplasia did not seem to play a critical role in the 
      pathogenesis of CP.
FAU - Era, Saho
AU  - Era S
AD  - Department of Health and Environmental Sciences, Kyoto University Graduate School 
      of Medicine, Yoshida Konoe, Sakyo-ku, Kyoto 6068501, Japan.
FAU - Harada, Kouji H
AU  - Harada KH
FAU - Toyoshima, Megumi
AU  - Toyoshima M
FAU - Inoue, Kayoko
AU  - Inoue K
FAU - Minata, Mutsuko
AU  - Minata M
FAU - Saito, Norimitsu
AU  - Saito N
FAU - Takigawa, Toshiya
AU  - Takigawa T
FAU - Shiota, Kouhei
AU  - Shiota K
FAU - Koizumi, Akio
AU  - Koizumi A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081112
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Alkanesulfonic Acids)
RN  - 0 (Anthraquinones)
RN  - 0 (Fluorocarbons)
RN  - 0 (Indicators and Reagents)
RN  - 60MEW57T9G (alizarin)
RN  - 9H2MAI21CL (perfluorooctane sulfonic acid)
RN  - P4448TJR7J (Alcian Blue)
SB  - IM
MH  - Alcian Blue
MH  - Alkanesulfonic Acids/pharmacokinetics/*toxicity
MH  - Amniotic Fluid/metabolism
MH  - Animals
MH  - Anthraquinones
MH  - Body Weight/drug effects
MH  - Cleft Palate/*chemically induced/*pathology
MH  - Female
MH  - Fetal Blood/metabolism
MH  - Fluorocarbons/pharmacokinetics/*toxicity
MH  - Indicators and Reagents
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Organ Culture Techniques
MH  - Organ Size/drug effects
MH  - Pregnancy
EDAT- 2008/12/02 09:00
MHDA- 2009/03/25 09:00
CRDT- 2008/12/02 09:00
PHST- 2008/10/11 00:00 [received]
PHST- 2008/11/02 00:00 [revised]
PHST- 2008/11/03 00:00 [accepted]
PHST- 2008/12/02 09:00 [entrez]
PHST- 2008/12/02 09:00 [pubmed]
PHST- 2009/03/25 09:00 [medline]
AID - S0300-483X(08)00522-2 [pii]
AID - 10.1016/j.tox.2008.11.003 [doi]
PST - ppublish
SO  - Toxicology. 2009 Feb 4;256(1-2):42-7. doi: 10.1016/j.tox.2008.11.003. Epub 2008 
      Nov 12.