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 CdCl₂/L) and/or Zn (ZnCl₂ 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.

进行这项研究以研究母体Cd和/或Zn暴露对Wistar大鼠胎儿脑中Zn代谢某些参数的影响。因此，雌性对照和其他在妊娠期通过口服途径暴露于Cd（50 mg CdCl ₂ / L）和/或Zn（ZnCl ₂使用60 mg / L）。处死妊娠20天（GD20）的雄性胎儿，并取其大脑进行组织学，化学和分子分析。在暴露于Cd的母亲的胎儿的大脑中观察到锌的消耗。组织学分析表明，与对照相比，Cd暴露可引起海马皮质区和CA1区的缩密症。在镉暴露下，我们注意到编码参与细胞内掺入锌的膜转运蛋白的基因（ZIP6）的过表达与抑制编码参与将锌输出到细胞外培养基（ZnT1和ZnT3）的转运蛋白的基因有关。镉组还发现与神经营养因子（BDNF）编码相关的基因的表达减少与金属调节转录因子1（MTF1）的过量表达有关，而金属调节转录因子1是与锌的体内稳态有关的因子。有趣的是，锌的供应完全或部分恢复了由镉暴露引起的变化。脑锌含量的减少以及编码膜锌转运蛋白的基因表达谱的改变，表明在胎儿脑中观察到的镉的毒性部分地由锌代谢的损害来介导。