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实验性朊病毒病中氧化应激的证据。

Evidence for oxidative stress in experimental prion disease.

作者信息

Guentchev M, Voigtländer T, Haberler C, Groschup M H, Budka H

机构信息

Austrian Reference Center for Human Prion Diseases and Institute of Neurology, University of Vienna, Vienna, A-1097, Austria.

出版信息

Neurobiol Dis. 2000 Aug;7(4):270-3. doi: 10.1006/nbdi.2000.0290.

DOI:10.1006/nbdi.2000.0290
PMID:10964599
Abstract

Oxidative stress has been shown to be important in several neurodegenerative disorders. Previous in vitro studies have already demonstrated the ability of a prion protein fragment to induce oxidative stress in cultured cells. By immunohistochemistry for nitrotyrosine (NT) and heme oxygenase-1 as markers for oxidative stress, we found widespread neuronal labeling for NT in scrapie-infected mouse brains, in agreement with peroxynitrite mediated neuronal degeneration. Damage by free radicals is a likely cause for neurodegeneration in prion disease, and antioxidants are a potential therapy of these disorders.

摘要

氧化应激已被证明在几种神经退行性疾病中起重要作用。先前的体外研究已经证明朊病毒蛋白片段能够在培养细胞中诱导氧化应激。通过免疫组织化学检测硝基酪氨酸(NT)和血红素加氧酶-1作为氧化应激的标志物,我们发现在羊瘙痒症感染的小鼠脑中广泛存在神经元NT标记,这与过氧亚硝酸盐介导的神经元变性一致。自由基损伤可能是朊病毒疾病中神经退行性变的一个原因,抗氧化剂是这些疾病的一种潜在治疗方法。

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