Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model

被引：60

作者：

Acs, P. ^{[1
]}

Selak, M. A. ^{[2
]}

Komoly, S. ^{[1
]}

Kalman, B. ^{[1
,3
]}

机构：

[1] Univ Pecs, Dept Neurol, H-7623 Pecs, Hungary

[2] Emergency Med Univ Penn, Sch Med, Philadelphia, PA USA

[3] Markusovszky Univ Hosp, Szombathely, Hungary

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2013年 / 262卷 / 1-2期

关键词：

Cuprizone; Copper chelation; Mitochondrial toxicity; Demyelination; Selective vulnerability; Multiple sclerosis; MULTIPLE-SCLEROSIS; SUPEROXIDE-DISMUTASE; REMYELINATION; HETEROGENEITY; PATHOGENESIS; PATHOLOGY; DECREASE; ASSAY;

D O I：

10.1016/j.jneuroim.2013.06.012

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：128 / 131

页数：4

共 21 条

[1] Preferential loss of myelin-associated glycoprotein reflects hypoxia-like white matter damage in stroke and inflammatory brain diseases [J].