Molecular mechanism of zinc-induced neurotoxicity : involvement of Ca and ER stress

锌（Zn）具有神经毒性，可引起短暂性全脑缺血后的神经退行性变，在血管性痴呆的发病机制中起重要作用。我们在体外研究了锌诱导神经毒性的分子机制。对锌诱导神经元死亡过程中上调基因的分析揭示了内质网应激的重要意义。这些新结果表明，钙离子稳态的破坏和内质网应激在锌诱导神经毒性的分子机制中，并有助于寻找血管性痴呆的保护物质。

Zinc(Zn) is neurotoxic and causes neurodegeneration following transient global ischemia and plays a crucial role in the pathogenesis of vascular-type dementia. We investigated the molecular mechanisms of Zn-induced neurotoxicity in vitro. The analysis of upregulated genes during Zn-induced neuronal death revealed that the significance of ER stress. These new results indicate that the disruption of Ca2+homeostasis and ER stress in the molecular mechanism of Zn-induced neurotoxicity, and are useful for the search for protective substances for vasucular dementia.