Effect of in utero exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis: A study in rats using different ways of administration

Yudai Kariyazono, Junki Taura, Yukiko Hattori, Yuji Ishii, Shizuo Narimatsu, Masatake Fujimura, Tomoki Takeda, Hideyuki Yamada

研究成果: ジャーナルへの寄稿レター

6 引用 (Scopus)

抄録

The effects of endocrine disruptors on testicular steroidogenesis in fetal rats were investigated in a study involving in utero exposure. In the major part of this study, pregnant rats at gestational day (GD)15 were given a single oral administration of the test substance, and then the expression of the following mRNAs in GD20 fetuses was determined: testicular steroidogenic acute-regulatory protein (StAR), a cholesterol transporter mediating the rate-limiting step of steroidogenesis, a ß-subunit of pituitary luteinizing hormone (LH), and a regulator of gonadal steroidogenesis. Among the substances tested, only di(2-ethylhexyl)phthalate (DEHP) reduced the expression of fetal testicular StAR. The others listed below exhibited little effect on fetal StAR: 2,2’,4,4’-tetrabromodiphenylether, tributyltin chloride, atrazine, permethrin, cadmium chloride (Cd), lead acetate (Pb) and methylmercury (CH3HgOH). None of them, including DEHP, lacked the ability to reduce the expression of pituitary LHß mRNA. The present study also examined the potential of metals as modifiers of fetal steroidogenesis by giving them to pregnant dams in drinking water during GD1 and GD20. Under these conditions, Cd and Pb at a low concentration (0.01 ppm) significantly attenuated the fetal testicular expression of StAR mRNA without a concomitant reduction in LHß. No such effect was detected with CH3HgOH even at 1 ppm. These results suggest that: 1) DEHP, Cd and Pb attenuate the fetal production of sex steroids by directly acting on the testis, and 2) chronic treatment during the entire gestational period is more useful than a single administration for determining the hazardous effect of a suspected endocrine disruptor on fetal steroidogenesis.

元の言語英語
ページ(範囲)909-916
ページ数8
ジャーナルJournal of Toxicological Sciences
40
発行部数6
DOI
出版物ステータス出版済み - 11 10 2015

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Endocrine Disruptors
Gonads
Rats
Luteinizing Hormone
Pituitary Hormones
Messenger RNA
Chlorides
Permethrin
Atrazine
Cadmium Chloride
Drinking Water
Dams
Oral Administration
Testis
Fetus
Metals
Steroids
Cholesterol
steroidogenic acute regulatory protein
phthalic acid

All Science Journal Classification (ASJC) codes

  • Toxicology

これを引用

Effect of in utero exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis : A study in rats using different ways of administration. / Kariyazono, Yudai; Taura, Junki; Hattori, Yukiko; Ishii, Yuji; Narimatsu, Shizuo; Fujimura, Masatake; Takeda, Tomoki; Yamada, Hideyuki.

:: Journal of Toxicological Sciences, 巻 40, 番号 6, 10.11.2015, p. 909-916.

研究成果: ジャーナルへの寄稿レター

Kariyazono, Yudai ; Taura, Junki ; Hattori, Yukiko ; Ishii, Yuji ; Narimatsu, Shizuo ; Fujimura, Masatake ; Takeda, Tomoki ; Yamada, Hideyuki. / Effect of in utero exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis : A study in rats using different ways of administration. :: Journal of Toxicological Sciences. 2015 ; 巻 40, 番号 6. pp. 909-916.
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abstract = "The effects of endocrine disruptors on testicular steroidogenesis in fetal rats were investigated in a study involving in utero exposure. In the major part of this study, pregnant rats at gestational day (GD)15 were given a single oral administration of the test substance, and then the expression of the following mRNAs in GD20 fetuses was determined: testicular steroidogenic acute-regulatory protein (StAR), a cholesterol transporter mediating the rate-limiting step of steroidogenesis, a {\ss}-subunit of pituitary luteinizing hormone (LH), and a regulator of gonadal steroidogenesis. Among the substances tested, only di(2-ethylhexyl)phthalate (DEHP) reduced the expression of fetal testicular StAR. The others listed below exhibited little effect on fetal StAR: 2,2’,4,4’-tetrabromodiphenylether, tributyltin chloride, atrazine, permethrin, cadmium chloride (Cd), lead acetate (Pb) and methylmercury (CH3HgOH). None of them, including DEHP, lacked the ability to reduce the expression of pituitary LH{\ss} mRNA. The present study also examined the potential of metals as modifiers of fetal steroidogenesis by giving them to pregnant dams in drinking water during GD1 and GD20. Under these conditions, Cd and Pb at a low concentration (0.01 ppm) significantly attenuated the fetal testicular expression of StAR mRNA without a concomitant reduction in LH{\ss}. No such effect was detected with CH3HgOH even at 1 ppm. These results suggest that: 1) DEHP, Cd and Pb attenuate the fetal production of sex steroids by directly acting on the testis, and 2) chronic treatment during the entire gestational period is more useful than a single administration for determining the hazardous effect of a suspected endocrine disruptor on fetal steroidogenesis.",
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AU - Ishii, Yuji

AU - Narimatsu, Shizuo

AU - Fujimura, Masatake

AU - Takeda, Tomoki

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