PMID- 20519845
OWN - NLM
STAT- MEDLINE
DCOM- 20100923
LR  - 20190911
IS  - 1880-3989 (Electronic)
IS  - 0388-1350 (Linking)
VI  - 35
IP  - 3
DP  - 2010 Jun
TI  - Maternal exposure to dioxin reduces hypothalamic but not pituitary metabolome in 
      fetal rats: a possible mechanism for a fetus-specific reduction in 
      steroidogenesis.
PG  - 365-73
AB  - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) reduces the synthesis of pituitary 
      gonadotropins in a fetal age-specific manner. The pituitary synthesis of 
      gonadotropins is regulated by the hypothalamus and, thus, needs the 
      differentiation and development of the hypothalamus requiring a number of factors 
      including energy supply and neurotransmitters. To investigate the mechanism 
      whereby TCDD reduces fetal gonadotropins, we carried out a comparative study on 
      the metabolomes of the hypothalamus and pituitary using fetal and mature Wistar 
      rats. Male fetuses at gestational day (GD)20 were removed from dams treated 
      orally with TCDD (1 microg/kg) at GD15, and the metabolome profiles were analyzed 
      by gas chromatography-mass spectrometry (GC-MS). The principal component analysis 
      of GC-MS data revealed that TCDD caused a change in the profile of fetal 
      metabolome more markedly in the hypothalamus than in the pituitary. In sharp 
      contrast, TCDD did not cause any marked alteration in hypothalamic as well as 
      pituitary metabolomes in male rats born of untreated dams and treated with TCDD 
      at postnatal day 49. It was also demonstrated that a number of fetal hypothalamic 
      components, including glutamine and gamma-aminobutyric acid, are reduced by TCDD. 
      These results demonstrate a possibility that TCDD may reduce the metabolic 
      activity of the hypothalamus in a fetus-specific fashion, resulting in the 
      reduced synthesis of gonadotropins.
FAU - Matsumoto, Yuki
AU  - Matsumoto Y
AD  - Graduate School of Pharmaceutical Sciences, Kyushu University, Maidashi, 
      Higashi-ku, Fukuoka, Japan. hyamada@phar.kyushu-u.ac.jp
FAU - Ishida, Takumi
AU  - Ishida T
FAU - Takeda, Tomoki
AU  - Takeda T
FAU - Koga, Takayuki
AU  - Koga T
FAU - Fujii, Misaki
AU  - Fujii M
FAU - Ishii, Yuji
AU  - Ishii Y
FAU - Fujimura, Yoshinori
AU  - Fujimura Y
FAU - Miura, Daisuke
AU  - Miura D
FAU - Wariishi, Hiroyuki
AU  - Wariishi H
FAU - Yamada, Hideyuki
AU  - Yamada H
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - J Toxicol Sci
JT  - The Journal of toxicological sciences
JID - 7805798
RN  - 0 (Gonadotropins)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0RH81L854J (Glutamine)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
SB  - IM
MH  - Animals
MH  - Depression, Chemical
MH  - Female
MH  - Gas Chromatography-Mass Spectrometry
MH  - Glutamine/metabolism
MH  - Gonadotropins/*biosynthesis
MH  - Hypothalamus/*metabolism
MH  - Male
MH  - Maternal Exposure/*adverse effects
MH  - *Maternal-Fetal Exchange
MH  - Metabolome/*drug effects
MH  - Pituitary Gland/metabolism
MH  - Polychlorinated Dibenzodioxins/*adverse effects
MH  - Pregnancy
MH  - Rats
MH  - Rats, Wistar
MH  - gamma-Aminobutyric Acid/metabolism
EDAT- 2010/06/04 06:00
MHDA- 2010/09/24 06:00
CRDT- 2010/06/04 06:00
PHST- 2010/06/04 06:00 [entrez]
PHST- 2010/06/04 06:00 [pubmed]
PHST- 2010/09/24 06:00 [medline]
AID - JST.JSTAGE/jts/35.365 [pii]
AID - 10.2131/jts.35.365 [doi]
PST - ppublish
SO  - J Toxicol Sci. 2010 Jun;35(3):365-73. doi: 10.2131/jts.35.365.