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镉诱导的卵巢病理生理学是通过斑马鱼(Danio rerio)中锌转运体基因表达模式的改变来介导的。

Cadmium-induced ovarian pathophysiology is mediated by change in gene expression pattern of zinc transporters in zebrafish (Danio rerio).

机构信息

Génétique, Biodiversité et Valorisation des Bioressources, Institut de Biotechnologie, Monastir, Tunisia.

出版信息

Chem Biol Interact. 2011 Sep 5;193(2):172-9. doi: 10.1016/j.cbi.2011.06.010. Epub 2011 Jul 3.

Abstract

This study explored the potential for expression pattern of genes encoding zinc (Zn) transporters to be involved in the cadmium (Cd)-induced reproductive toxicity in female of zebrafish. For this purpose, oocytes maturity and ovarian histology as well as Cd, Zn and metallothioneins (MTs) accumulation and expression of genes encoding Zrt-,Irt-related protein 10 (ZIP10), Zn transporter 1 (ZnT1) and zebrafish metallothionein (zMT) were examined in ovaries of adult zebrafish exposed to 0.4 mg/L Cd in water and supplemented with Zn (5 mgkg(-1)) in their diet for 21 days. Cd-exposure decreased the expression of ZnT1 and caused up-regulation of ZIP10 and zMT gene expression. These changes were accompanied by increased Cd and MTs accumulation, decreased Zn contents as well as by histopathological damages in ovarian tissues. The co-exposure of fish to Cd and Zn abolished ZnT1 down-regulation and rendered a persistently increased ZIP10 mRNA level. This treatment also decreased Cd and MTs accumulation, reversed Cd-induced Zn depletion and partially restored Cd-induced histological changes in ovarian tissues. These results imply that the downregulation of ZnT1 as well as the overexpression of ZIP10, in responses to the ovarian Zn depletion induced by Cd, play a major role in Cd accumulation and consequently in its toxicity. The protective effect of dietary Zn supplementation against Cd-induced toxicity is mediated, at least in part, by the increase of Zn availability and subsequently the induction of ZnT1 gene expression.

摘要

本研究旨在探讨编码锌(Zn)转运体的基因表达模式是否参与镉(Cd)诱导的斑马鱼雌性生殖毒性。为此,我们检测了暴露于水中 0.4mg/L Cd 并在饮食中补充 5mg/kg Zn 的成年斑马鱼的卵母细胞成熟度和卵巢组织学以及 Cd、Zn 和金属硫蛋白(MTs)的积累,以及编码 Zrt-、Irt 相关蛋白 10(ZIP10)、Zn 转运体 1(ZnT1)和斑马鱼金属硫蛋白(zMT)的基因表达。Cd 暴露降低了 ZnT1 的表达,并导致 ZIP10 和 zMT 基因表达上调。这些变化伴随着 Cd 和 MTs 积累增加、Zn 含量降低以及卵巢组织的组织病理学损伤。鱼类同时暴露于 Cd 和 Zn 会消除 ZnT1 的下调,并使 ZIP10 mRNA 水平持续升高。这种处理还降低了 Cd 和 MTs 的积累,逆转了 Cd 引起的 Zn 耗竭,并部分恢复了 Cd 引起的卵巢组织的组织学变化。这些结果表明,ZnT1 的下调以及 ZIP10 的过度表达,作为对 Cd 诱导的卵巢 Zn 耗竭的反应,在 Cd 积累及其毒性中起主要作用。膳食 Zn 补充对 Cd 诱导的毒性的保护作用至少部分是通过增加 Zn 的可用性并随后诱导 ZnT1 基因表达来介导的。

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