PMID- 23858793
OWN - NLM
STAT- MEDLINE
DCOM- 20131104
LR  - 20161125
IS  - 0016-254X (Print)
IS  - 0016-254X (Linking)
VI  - 104
IP  - 4
DP  - 2013 Apr
TI  - [The gender-specific effect of maternal exposure to dioxin on fetal 
      steroidogenesis in the adrenal gland].
PG  - 143-51
AB  - Maternal exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) causes a 
      number of toxic effects on development such as growth retardation and sexual 
      immaturity in the offspring. However, the toxic mechanism remains unknown. Our 
      previous studies have revealed that single oral administration of TCDD (1 jg/kg) 
      to pregnant rats at gestational day (GD) 15 attenuates the fetal expression of 
      testicular steroidogenic proteins such as steroidogenic acute-regulatory protein 
      (StAR) and cytochrome P450 (CYP) 17 by targeting the fetal production of 
      pituitary gonadotropins. In addition, we provided evidence that TCDD-produced 
      damage on the fetal pituitary-gonad axis leads to imprint defects in sexual 
      behaviors at adulthood. In this study, we investigated whether TCDD also affects 
      fetal steroidogenesis in the adrenal gland. When pregnant Wistar rats were orally 
      treated with TCDD, the fetal expression of CYP21, CYP11B1 and CYP11B2 mRNAs was 
      either induced or tended to be induced in the male adrenal gland during GD17 and 
      GD19, while the expression of mRNAs coding for StAR, CYP11A1 and 
      313-hydroxysteroid dehydrogenase was insensitive to TCDD treatment. The above 
      alterations did not seem to be caused through a change in the upstream regulator, 
      because TCDD exhibited little ability to attenuate the expression of 
      adrenocorticotropin, a pituitary hormone stimulating adrenal steroidogenesis, in 
      the male and female fetuses. In contrast to the males, TCDD effect on the adrenal 
      gland was not observed in the female fetuses. These results suggest that maternal 
      exposure to TCDD disrupts fetal steroidogenesis in adrenal as well as gonadal 
      glands in a male specific manner, and the mechanism underlying the effect on 
      adrenal gland is independent of the alteration of pituitary regulator.
FAU - Takeda, Tomoki
AU  - Takeda T
AD  - Graduate School of Pharmaceutical Sciences, Kyushu University.
FAU - Hattori, Yukiko
AU  - Hattori Y
FAU - Fujii, Misaki
AU  - Fujii M
FAU - Taura, Junki
AU  - Taura J
FAU - Ishi, Yuji
AU  - Ishi Y
FAU - Yamada, Hideyuki
AU  - Yamada H
LA  - jpn
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Fukuoka Igaku Zasshi
JT  - Fukuoka igaku zasshi = Hukuoka acta medica
JID - 9423321
RN  - 0 (Gonadal Steroid Hormones)
RN  - 0 (Polychlorinated Dibenzodioxins)
SB  - IM
MH  - Adrenal Glands/*drug effects/*metabolism
MH  - Animals
MH  - Female
MH  - Fetus/*drug effects/metabolism
MH  - Gonadal Steroid Hormones/*biosynthesis
MH  - Male
MH  - *Maternal Exposure
MH  - Polychlorinated Dibenzodioxins/*toxicity
MH  - Pregnancy
MH  - Rats
MH  - Rats, Wistar
MH  - Sex Factors
EDAT- 2013/07/19 06:00
MHDA- 2013/11/05 06:00
CRDT- 2013/07/18 06:00
PHST- 2013/07/18 06:00 [entrez]
PHST- 2013/07/19 06:00 [pubmed]
PHST- 2013/11/05 06:00 [medline]
PST - ppublish
SO  - Fukuoka Igaku Zasshi. 2013 Apr;104(4):143-51.