PMID- 21706896
OWN - NLM
STAT- MEDLINE
DCOM- 20110728
LR  - 20161125
IS  - 0016-254X (Print)
IS  - 0016-254X (Linking)
VI  - 102
IP  - 4
DP  - 2011 Apr
TI  - [The effect of maternal exposure to dioxin on fetal steroidogenesis in the 
      steroidogenic organs].
PG  - 159-66
AB  - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposed to pregnant or lactational 
      mother impairs the reproduction and development of the pups. The defect is a 
      serious problem, because it is caused by TCDD at much lower doses than that 
      needed for acute toxicity in the mother. However, the toxic mechanism underlying 
      the defect remains to be obscure. We have previously revealed that maternal 
      exposure to TCDD (1 microg/kg) causes a reduction in luteinizing hormone in the 
      fetal pituitary, leading to the reduced expression of testicular steroidogenic 
      proteins such as steroidogenic acute-regulatory protein (StAR) and cytochrome 
      P450 (CYP) 17. In addition, we have provided evidence that such a reduction 
      imprints defects in sexual behaviors at adulthood. In this study, we investigated 
      TCDD effect on fetal steroidogenesis in the extra-gonadal tissues. Even when 
      pregnant Wistar rats at gestational day (GD) 15 were orally treated with TCDD 
      (0.25, 1 or 3 microg/kg), neither expression of StAR nor CYP17 mRNA was affected 
      in the adrenal gland, placenta and hypothalamus of male fetuses (GD20). However, 
      TCDD induced placental StAR (3 microg/kg) and adrenal CYP17 mRNAs (0.25 
      microg/kg) in female fetuses. Therefore, our study suggests that while TCDD gives 
      damage to male fetal steroidogenesis in a testis-specific manner, the dioxin 
      enhances the steroidogenesis of the fetal adrenal gland and placenta in females. 
      Thus, the mechanism whereby TCDD exerts its endocrine-disrupting properties is 
      considered to differ, at least partially, between male and female fetuses.
FAU - Takeda, Tomoki
AU  - Takeda T
AD  - Graduate School of Pharmaceutical Sciences, Kyushu University.
FAU - Taura, Junki
AU  - Taura J
FAU - Fujii, Misaki
AU  - Fujii M
FAU - Koga, Takayuki
AU  - Koga T
FAU - Ishii, Yuji
AU  - Ishii 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 (Phosphoproteins)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0 (Steroids)
RN  - 0 (steroidogenic acute regulatory protein)
RN  - EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase)
SB  - IM
MH  - Adrenal Glands/*metabolism
MH  - Animals
MH  - Female
MH  - Fetus/*metabolism
MH  - Male
MH  - *Maternal Exposure
MH  - Phosphoproteins/metabolism
MH  - Placenta/*metabolism
MH  - Polychlorinated Dibenzodioxins/*poisoning
MH  - Pregnancy
MH  - Rats
MH  - Rats, Wistar
MH  - Sex Factors
MH  - Steroid 17-alpha-Hydroxylase/metabolism
MH  - Steroids/*biosynthesis
EDAT- 2011/06/29 06:00
MHDA- 2011/07/29 06:00
CRDT- 2011/06/29 06:00
PHST- 2011/06/29 06:00 [entrez]
PHST- 2011/06/29 06:00 [pubmed]
PHST- 2011/07/29 06:00 [medline]
PST - ppublish
SO  - Fukuoka Igaku Zasshi. 2011 Apr;102(4):159-66.