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培养的大鼠小脑颗粒神经元中锌离子的毒性作用伴随着细胞质酸化。

Toxic Effect of Zinc Ions Is Accompanied by Acidification of the Cytoplasm in Cultured Rat Cerebellar Granule Neurons.

机构信息

Research Center of Neurology, Moscow, Russia.

M. V. Lomonosov Moscow State University, Moscow, Russia.

出版信息

Bull Exp Biol Med. 2022 Aug;173(4):539-543. doi: 10.1007/s10517-022-05578-0. Epub 2022 Sep 5.

DOI:10.1007/s10517-022-05578-0
PMID:36058978
Abstract

Addition of 0.07 mM zinc ions to the culture medium induced death of cerebellar granule neurons. This was preceded by a decrease in intracellular pH by 0.86±0.12 and an increase in the level of intracellular zinc registered by increasing fluorescence of FluoZin3. However, intracellular acidosis caused by acidification of the culture medium to pH 6.0 was not toxic to neurons, and even significantly increased their survival under the action of zinc ions. In general, the overload of the neurons cytoplasm with zinc ions causes acidification of the cytoplasm, which is probably associated with the activation of Zn2/H exchangers and is a protective mechanism for the neurocytotoxic effect of zinc ions.

摘要

向培养基中添加 0.07 mM 的锌离子会诱导小脑颗粒神经元死亡。这是由细胞内 pH 值下降 0.86±0.12 和 FluoZin3 荧光强度增加所记录到的细胞内锌水平升高所引起的。然而,将培养基酸化至 pH 6.0 引起的细胞内酸中毒对神经元并无毒性,甚至在锌离子的作用下显著增加了神经元的存活率。总的来说,锌离子使神经元细胞质超载会导致细胞质酸化,这可能与 Zn2+/H+交换器的激活有关,是锌离子神经细胞毒性作用的一种保护机制。

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引用本文的文献

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Extracellular Acidosis, Cysteine, and Glutathione Enhance the Toxic Effect of Copper Ions in Cultures of Cerebellar Granule Neurons.细胞外酸中毒、半胱氨酸和谷胱甘肽增强小脑颗粒神经元培养物中铜离子的毒性作用。
Bull Exp Biol Med. 2024 Sep;177(5):588-591. doi: 10.1007/s10517-024-06229-2. Epub 2024 Sep 28.

本文引用的文献

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ZnT2 is an electroneutral proton-coupled vesicular antiporter displaying an apparent stoichiometry of two protons per zinc ion.ZnT2 是一种电中性质子偶联囊泡转运体,每转运一个锌离子显示出 2 个质子的表观协同转运比。
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Zinc as a Neuromodulator in the Central Nervous System with a Focus on the Olfactory Bulb.锌作为中枢神经系统中的神经调节剂,重点关注嗅球。
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锌的神经毒性
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Role of acidosis, NMDA receptors, and acid-sensitive ion channel 1a (ASIC1a) in neuronal death induced by ischemia.酸中毒、N-甲基-D-天冬氨酸受体及酸敏感离子通道1a(ASIC1a)在缺血诱导的神经元死亡中的作用
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Brain Res Rev. 2009 Mar;59(2):347-73. doi: 10.1016/j.brainresrev.2008.10.003. Epub 2008 Nov 7.