LR11ES41: Génétique, Biodiversité et Valorisation des Bioressources, Institut de Biotechnologie, Université de Monastir, 5000 Monastir, Tunisia.
LR11ES41: Génétique, Biodiversité et Valorisation des Bioressources, Institut de Biotechnologie, Université de Monastir, 5000 Monastir, Tunisia.
Chem Biol Interact. 2018 Apr 25;286:88-95. doi: 10.1016/j.cbi.2018.03.005. Epub 2018 Mar 14.
This study was carried out to investigate the effects of maternal Cd and/or Zn exposure on some parameters of Zn metabolism in fetal brain of Wistar rats. Thus, female controls and other exposed by the oral route during the gestation period to Cd (50 mg CdCl/L) and/or Zn (ZnCl 60 mg/L) were used. The male fetuses at age 20 days of gestation (GD20) were sacrificed and their brains were taken for histological, chemical and molecular analysis. Zn depletion was observed in the brains of fetuses issued from mothers exposed to Cd. Histological analysis showed that Cd exposure induces pyknosis in cortical region and CA1 region of the hippocampus compared to controls. Under Cd exposure, we noted an overexpression of the genes coding for membrane transporter involved in the intracellular incorporation of Zn (ZIP6) associated with inhibition of that encoding the transporters involved in the output of the Zn into the extracellular medium (ZnT1 and ZnT3). A decrease in the expression of the gene encoding the neuro-trophic factor (BDNF) associated with overexpression of the encoding the metal regulatory transcription factor 1 (MTF1), factor involved in the homeostasis of Zn, was also noted in Cd group. Interestingly, Zn supply provided a total or partial restauration of the changes induced by the Cd exposure. The depletion of brain Zn contents as well as the modification of the profile of expression of genes encoding membrane Zn transporters, suggest that the toxicity of Cd observed in fetal brain level are mediated, in part, by impairment of Zn metabolism.
本研究旨在探讨母体镉（Cd）和/或锌（Zn）暴露对 Wistar 大鼠胎儿大脑中 Zn 代谢某些参数的影响。因此，雌性对照组和其他通过口服途径在妊娠期暴露于 Cd（50mg CdCl/L）和/或 Zn（ZnCl 60mg/L）的动物被用于本研究。在妊娠第 20 天（GD20）处死雄性胎儿，并取出其大脑进行组织学、化学和分子分析。从暴露于 Cd 的母体中娩出的胎儿大脑中观察到 Zn 耗竭。组织学分析显示，与对照组相比，Cd 暴露会导致皮质区和海马 CA1 区的核固缩。在 Cd 暴露下，我们注意到编码参与细胞内 Zn 摄取的膜转运体的基因（ZIP6）的过度表达，同时伴有编码将 Zn 输出到细胞外介质的转运体的基因（ZnT1 和 ZnT3）的抑制。此外，还观察到编码神经营养因子（BDNF）的基因表达降低，同时编码金属调节转录因子 1（MTF1）的基因表达增加，MTF1 是参与 Zn 体内平衡的因子。有趣的是，Zn 供应提供了 Cd 暴露引起的变化的完全或部分恢复。大脑 Zn 含量的耗竭以及编码膜 Zn 转运体的基因表达谱的改变提示，在胎儿大脑水平观察到的 Cd 毒性部分是通过损害 Zn 代谢介导的。
