Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model
Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model
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DOI：
10.1016/j.jneuroim.2013.06.012
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发表时间：
2013-09-15
影响因子：
3.3
通讯作者：
Kalman, B.
中科院分区：
文献类型：
--
作者：
Acs, P.;Selak, M. A.;Kalman, B.
Cuprizone是一种螯合铜的线粒体毒素，其优先在C57 BL/6小鼠的胼胝体（CC）和上级小脑脚中引起少突胶质细胞凋亡和脱髓鞘，但不在脊髓（SC）中。在这里，我们的目的是确定含铜酶的活动与脱髓鞘的分布在暴露于cuprizone。这项研究揭示了线粒体复合物IV和超氧化物歧化酶活性的改变，在病理影响的CC和不受影响的SC。这一观察结果提出了区域不同的亚细胞分子相互作用的可能性，导致选择性少突胶质细胞损失诱导的非选择性线粒体毒素，cuprizone。(C)2013爱思唯尔有限公司版权所有。
Cuprizone is a copper-chelating mitochondrial toxin that causes oligodendrocyte apoptosis and demyelination preferentially in the corpus callosum (CC) and the superior cerebellar peduncles, but not in the spinal cord (SC) of C57BL/6 mice. Here we aimed to determine the activities of copper-containing enzymes in correlation with the distribution of demyelination during exposure to cuprizone. The study revealed mitochondrial complex IV and superoxide dismutase activity alterations in both the pathology-affected CC and the non-affected SC. This observation raises the possibility that regionally different subcellular molecular interactions lead to the selective oligodendrocyte loss induced by the nonselective mitochondrial toxin, cuprizone. (C) 2013 Elsevier B.V. All rights reserved.