カドミウムの母子間移行におけるメタロチオネインと金属トランスポーターの役割

  • 深瀬 陽平
    北里大学医療系大学院環境医科学群環境毒医科学
  • 津上 尚士
    北里大学医療系大学院環境医科学群環境毒医科学
  • 中村 康宏
    北里大学医療衛生学部衛生管理学産業保健学
  • 大場 謙一
    北里大学医療衛生学部衛生管理学産業保健学
  • 太田 久吉
    北里大学医療系大学院環境医科学群環境毒医科学 北里大学医療衛生学部衛生管理学産業保健学

書誌事項

タイトル別名
  • The Role of Metallothionein and Metal Transporter on Cadmium Transport from Mother to Fetus
  • Symposium Review : カドミウムの母子間移行におけるメタロチオネインと金属トランスポーターの役割
  • Symposium Review : カドミウム ノ ボシ カン イコウ ニ オケル メタロチオネイン ト キンゾク トランスポーター ノ ヤクワリ

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抄録

  We examined the role of Metallothionein (MT) and metal transporter on Cadmium (Cd) transport from mother to fetus. In this study, female Wistar rats were given Cd (as CdCl2) at a dose of 0, 1, 2 and 5 mg Cd/kg/d. Animals were sacrificed on the pregnant 19-21 d. The concentrations of Cd and MT, and gene expression of MT and metal transporters were determined in the placenta and in the fetuses. In mother rats, the concentration of Cd in the placenta increased dose-dependently, significantly. The Cd of MT-Cd form and the Cd of non-MT-Cd form increased also dose-dependently. In pathological examination of placenta tissue, syncytial trophoblast cells were damaged dose-dependently, particularly in 5 mg Cd/kg group. In fetuses, the Cd concentration in the total body, liver and kidney increased dose-dependently. The Cd concentration in liver of fetus was significantly higher than that in kidney. In gene expression of metal transporter, gene expression of Zip-8 and ATP7B increased dose-dependently in placenta in 0 mg, 1 mg and 2 mg groups, but the increase was not statistically significant. Based on these results, it was speculated that Cd in placenta is trapped to transport into fetus by MT in placenta. However, non-bound Cd by MT is leaked to fetus by damage of placenta tissue, and it was speculated that non-MT-Cd accumulated in liver of fetus. Namely, it was suggested the possibility that the non-bound Cd by MT is transported by metal transporter of zinc and copper, especially Zip-8 and ATP7B or leaked from the placenta as caused by damage of synsytial trophoblast.<br>

収録刊行物

  • 薬学雑誌

    薬学雑誌 134 (7), 801-804, 2014-07-01

    公益社団法人 日本薬学会

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