Accumulation of oxidative stress around the stroke-like lesions of MELAS patients
Accumulation of oxidative stress around the stroke-like lesions of MELAS patients
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DOI：
10.1016/j.mito.2009.04.002
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发表时间：
2009-09-01
期刊：
影响因子：
4.4
通讯作者：
Kashiwagi, Atsunori
中科院分区：
文献类型：
--
作者：
Katayama, Yuri;Maeda, Kengo;Kashiwagi, Atsunori
为了研究氧化应激与线粒体肌病、脑病、乳酸酸中毒和3243 A>G突变卒中样发作（MELAS）中卒中样病变进行性扩散之间的关系，我们回顾性分析了接受和未接受自由基清除剂依达拉奉治疗的患者的扩散频率。氧化损伤和防御酶进行了组织学评价。在接受依达拉奉治疗的患者中，扩散的频率显著降低。DNA氧化损伤的标志物8-羟基-2 '-脱氧鸟苷在损伤周围存活的神经元中明显蓄积，但锰超氧化物歧化酶和8-氧代鸟嘌呤糖基化酶1在损伤周围存活的神经元中未表达上调。氧化应激增加和防御不足可能参与了MELAS扩散性病变的发病机制。(C)2009年爱思唯尔B。和线粒体研究学会。All rights reserved.
To investigate the relationship between oxidative stress and progressive spread of the stroke-like lesions in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with 3243A>G mutation, we retrospectively analyzed the spread frequency in patients with and without treatment with the radical scavenger edaravone. Oxidative damage and defensive enzymes were histologically evaluated. Spread was significantly less frequent in the patients treated with edaravone. Although 8-hydroxy-2'-deoxyguanosine, a marker for oxidative damage of DNA, was obviously accumulated in peri-lesional surviving neurons, manganese superoxide dismutase and 8-oxoguanine glycosylase 1 were not up-regulated in those neurons. Increased oxidative stress and insufficient defense could be involved in the pathogenesis of the spreading lesions in MELAS. (C) 2009 Elsevier B. V. and Mitochondria Research Society. All rights reserved.