Xanthine oxidoreductase and neurological sequelae of carbon monoxide poisoning
Xanthine oxidoreductase and neurological sequelae of carbon monoxide poisoning
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DOI：
10.1016/j.toxlet.2007.02.006
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发表时间：
2007-04-25
影响因子：
3.5
通讯作者：
Thom, Stephen R.
中科院分区：
文献类型：
--
作者：
Han, Shih-Tsung;Bhopale, Veena M.;Thom, Stephen R.
神经系统后遗症（NS）是一氧化碳（CO）中毒的常见并发症，髓鞘碱性蛋白的结构改变已被证明是引发导致NS的免疫反应的原因。为了确定黄嘌呤氧化还原酶（XOR）是否参与CO介导的NS的病理生理学，我们检测了髓鞘碱性蛋白在CO中毒XOR耗尽大鼠和进行径向迷宫研究，以评估认知功能的改变。一氧化碳中毒的XOR耗尽大鼠没有表现出髓鞘碱性蛋白改变或认知功能受损，这两个发现在CO中毒的对照组大鼠。这些结果表明，XOR是必不可少的病理级联CO介导的NS。(C)2007爱思唯尔爱尔兰有限公司保留所有权利。
Neurological sequelae (NS) is a common complication of carbon monoxide (CO) poisoning and structural alterations of myelin basic protein have been proven to initiate immunological reactions leading to NS. To determine whether xanthine oxidoreductase (XOR) participates in the pathophysiology of CO-mediated NS, we examined myelin basic protein in CO poisoned XOR-depleted rats and performed radial maze studies to evaluate the alteration of cognitive function. Carbon monoxide poisoned XOR-depleted rats did not exhibit myelin basic protein alterations or impaired cognitive function, both found in CO poisoned control rats. These results indicate that XOR is essential to the pathological cascade of CO-mediated NS. (C) 2007 Elsevier Ireland Ltd. All rights reserved.