A. N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, 119992 Moscow, Russia.
Toxicol Lett. 2012 Jan 5;208(1):36-40. doi: 10.1016/j.toxlet.2011.10.003. Epub 2011 Oct 10.
Zinc chloride (0.01 mM kept for 3h) is not toxic to cultured cerebellar granule neurons (CGNs) while kainate (0.1mM kept for 3h) demonstrates some but very low toxicity towards these cells. Measurements of the relative intraneuronal zinc ion concentration showed that increase in Zn(2+) under the simultaneous action of ZnCl(2) and kainate was significantly stronger compared to their separate action. Simultaneous treatment of CGNs with kainate and zinc chloride caused the swelling of neuronal mitochondria and consequent intensive neuronal death, which was totally prevented by NBQX (an AMPA/kainate-receptors blocker) or ruthenium red (a mitochondrial Ca(2+) uniporter blocker). These data imply that Zn(2+) synergistically to kainate increase their separate toxic effects on mitochondria leading to rapid neuronal death.
氯化锌（0.01mM 孵育 3h）对培养的小脑颗粒神经元（CGNs）没有毒性，而红藻氨酸（0.1mM 孵育 3h）对这些细胞显示出一定但很低的毒性。对细胞内锌离子浓度的相对测量表明，与单独作用相比，氯化锌和红藻氨酸同时作用下 Zn(2+) 的增加明显更强。同时用红藻氨酸和氯化锌处理 CGNs 会导致神经元线粒体肿胀，继而导致神经元死亡，而 NBQX（AMPA/kainate 受体阻滞剂）或钌红（线粒体 Ca(2+) 单向转运体阻滞剂）完全阻止了这种情况。这些数据表明，Zn(2+) 与红藻氨酸协同作用，增加了它们对线粒体的单独毒性作用，导致神经元迅速死亡。
