2,3,4,7,8-Pentachlorodibenzofuran is far less potent than 2,3,7,8-tetrachlorodibenzo-p-dioxin in disrupting the pituitary-gonad axis of the rat fetus

Junki Taura, Tomoki Takeda, Misaki Fujii, Yukiko Hattori, Yuji Ishii, Hiroaki Kuroki, Kiyomi Tsukimori, Hiroshi Uchi, Masutaka Furue, Hideyuki Yamada

研究成果: ジャーナルへの寄稿記事

4 引用 (Scopus)

抄録

The effect of 2,3,4,7,8-pentachlorodibenzofuran (PnCDF) on the fetal pituitary-gonad axis was compared with that produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Wistar rats. Maternal treatment at gestational day (GD) 15 with PnCDF and TCDD reduced the fetal expression at GD20 of pituitary luteinizing hormone (LH) and the testicular proteins necessary for steroidogenesis. The relative potencies of PnCDF ranged from 1/42nd to 1/63rd of the TCDD effect. While PnCDF, at a dose sufficient to cause a reduction in fetal LH, provoked defects in sexual behavior at adulthood, a dose less than the ED50 failed to produce any abnormality. There was a loss of fetal body weight following in utero exposure to PnCDF, and the effect of PnCDF was also much less than that of TCDD. The disturbance in fetal growth was suggested to be due to a reduction in the level of fetal growth hormone (GH) by dioxins. The disorder caused by PnCDF/TCDD in the fetal pituitary-gonad axis occurred at doses less than those needed to cause wasting syndrome in pubertal rats. The harmful effect of PnCDF relative to TCDD was more pronounced in fetal rats than in pubertal rats. These lines of evidence suggest that: 1) PnCDF as well as TCDD imprints defects in sexual behavior by disrupting the fetal pituitary-gonad axis; 2) these dioxins hinder fetal growth by reducing the expression of fetal GH; and 3) the fetal effects of PnCDF/TCDD are more sensitive than sub-acute toxicity during puberty, and the relative effect of PnCDF varies markedly depending on the indices used.

元の言語英語
ページ(範囲)48-57
ページ数10
ジャーナルToxicology and Applied Pharmacology
281
発行部数1
DOI
出版物ステータス出版済み - 11 5 2014

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Gonads
Rats
Fetus
Fetal Development
Dioxins
Luteinizing Hormone
Sexual Behavior
Growth Hormone
Multifetal Pregnancy Reduction
Wasting Syndrome
Defects
Fetal Weight
Pituitary Hormones
2,3,4,7,8-pentachlorodibenzofuran
Polychlorinated Dibenzodioxins
1,4-dioxin
Puberty
Toxicity
Wistar Rats
Mothers

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology

これを引用

2,3,4,7,8-Pentachlorodibenzofuran is far less potent than 2,3,7,8-tetrachlorodibenzo-p-dioxin in disrupting the pituitary-gonad axis of the rat fetus. / Taura, Junki; Takeda, Tomoki; Fujii, Misaki; Hattori, Yukiko; Ishii, Yuji; Kuroki, Hiroaki; Tsukimori, Kiyomi; Uchi, Hiroshi; Furue, Masutaka; Yamada, Hideyuki.

:: Toxicology and Applied Pharmacology, 巻 281, 番号 1, 05.11.2014, p. 48-57.

研究成果: ジャーナルへの寄稿記事

Taura, Junki ; Takeda, Tomoki ; Fujii, Misaki ; Hattori, Yukiko ; Ishii, Yuji ; Kuroki, Hiroaki ; Tsukimori, Kiyomi ; Uchi, Hiroshi ; Furue, Masutaka ; Yamada, Hideyuki. / 2,3,4,7,8-Pentachlorodibenzofuran is far less potent than 2,3,7,8-tetrachlorodibenzo-p-dioxin in disrupting the pituitary-gonad axis of the rat fetus. :: Toxicology and Applied Pharmacology. 2014 ; 巻 281, 番号 1. pp. 48-57.
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abstract = "The effect of 2,3,4,7,8-pentachlorodibenzofuran (PnCDF) on the fetal pituitary-gonad axis was compared with that produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Wistar rats. Maternal treatment at gestational day (GD) 15 with PnCDF and TCDD reduced the fetal expression at GD20 of pituitary luteinizing hormone (LH) and the testicular proteins necessary for steroidogenesis. The relative potencies of PnCDF ranged from 1/42nd to 1/63rd of the TCDD effect. While PnCDF, at a dose sufficient to cause a reduction in fetal LH, provoked defects in sexual behavior at adulthood, a dose less than the ED50 failed to produce any abnormality. There was a loss of fetal body weight following in utero exposure to PnCDF, and the effect of PnCDF was also much less than that of TCDD. The disturbance in fetal growth was suggested to be due to a reduction in the level of fetal growth hormone (GH) by dioxins. The disorder caused by PnCDF/TCDD in the fetal pituitary-gonad axis occurred at doses less than those needed to cause wasting syndrome in pubertal rats. The harmful effect of PnCDF relative to TCDD was more pronounced in fetal rats than in pubertal rats. These lines of evidence suggest that: 1) PnCDF as well as TCDD imprints defects in sexual behavior by disrupting the fetal pituitary-gonad axis; 2) these dioxins hinder fetal growth by reducing the expression of fetal GH; and 3) the fetal effects of PnCDF/TCDD are more sensitive than sub-acute toxicity during puberty, and the relative effect of PnCDF varies markedly depending on the indices used.",
author = "Junki Taura and Tomoki Takeda and Misaki Fujii and Yukiko Hattori and Yuji Ishii and Hiroaki Kuroki and Kiyomi Tsukimori and Hiroshi Uchi and Masutaka Furue and Hideyuki Yamada",
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T1 - 2,3,4,7,8-Pentachlorodibenzofuran is far less potent than 2,3,7,8-tetrachlorodibenzo-p-dioxin in disrupting the pituitary-gonad axis of the rat fetus

AU - Taura, Junki

AU - Takeda, Tomoki

AU - Fujii, Misaki

AU - Hattori, Yukiko

AU - Ishii, Yuji

AU - Kuroki, Hiroaki

AU - Tsukimori, Kiyomi

AU - Uchi, Hiroshi

AU - Furue, Masutaka

AU - Yamada, Hideyuki

PY - 2014/11/5

Y1 - 2014/11/5

N2 - The effect of 2,3,4,7,8-pentachlorodibenzofuran (PnCDF) on the fetal pituitary-gonad axis was compared with that produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Wistar rats. Maternal treatment at gestational day (GD) 15 with PnCDF and TCDD reduced the fetal expression at GD20 of pituitary luteinizing hormone (LH) and the testicular proteins necessary for steroidogenesis. The relative potencies of PnCDF ranged from 1/42nd to 1/63rd of the TCDD effect. While PnCDF, at a dose sufficient to cause a reduction in fetal LH, provoked defects in sexual behavior at adulthood, a dose less than the ED50 failed to produce any abnormality. There was a loss of fetal body weight following in utero exposure to PnCDF, and the effect of PnCDF was also much less than that of TCDD. The disturbance in fetal growth was suggested to be due to a reduction in the level of fetal growth hormone (GH) by dioxins. The disorder caused by PnCDF/TCDD in the fetal pituitary-gonad axis occurred at doses less than those needed to cause wasting syndrome in pubertal rats. The harmful effect of PnCDF relative to TCDD was more pronounced in fetal rats than in pubertal rats. These lines of evidence suggest that: 1) PnCDF as well as TCDD imprints defects in sexual behavior by disrupting the fetal pituitary-gonad axis; 2) these dioxins hinder fetal growth by reducing the expression of fetal GH; and 3) the fetal effects of PnCDF/TCDD are more sensitive than sub-acute toxicity during puberty, and the relative effect of PnCDF varies markedly depending on the indices used.

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