Oxidative damage induced by the injection of HIV-1 Tat protein in the rat striatum
Oxidative damage induced by the injection of HIV-1 Tat protein in the rat striatum
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DOI：
10.1016/s0304-3940(01)01786-4
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发表时间：
2001-06-01
影响因子：
2.5
通讯作者：
Booze, RM
中科院分区：
文献类型：
--
作者：
Aksenov, MY;Hasselrot, U;Booze, RM
氧化应激已被假设在不同的神经退行性疾病，包括艾滋病毒相关的痴呆症的发病机制中发挥作用。达特是HIV的一种非结构蛋白，通过破坏钙稳态和氧化应激机制参与神经元凋亡的增强。注射焦油引起大鼠纹状体蛋白质羰基形成增加。蛋白质的氧化修饰增加发生在达特注射后早期，并在Tat介导的星形胶质细胞增生之前。脑切片的免疫染色表明，一个突出的蛋白质羰基免疫反应性的区域周围的注射部位在纹状体的Tat注射大鼠。强烈的蛋白质羰基免疫反应定位于细胞体。我们的研究表明，蛋白质氧化增加可能是达特神经毒性机制的重要组成部分。(C)2001爱思唯尔科学爱尔兰有限公司保留所有权利。
Oxidative stress has been hypothesized to play a role in the pathogenesis of different neurodegenerative disorders, including HIV-related dementia. Tat, a nonstructural protein of HIV, is implicated in potentiation of neuronal apoptosis by mechanisms involving the disruption of calcium homeostasis and oxidative stress. The injection of Tar caused an increase of protein carbonyl formation in the rat striatum. Increased oxidative modification of proteins occurred early after Tat injection and preceded Tat-mediated astrogliosis. Immunostaining of brain sections demonstrated that an area of prominent protein carbonyl immunoreactivity surrounded an injection site in the striatum of Tat-injected rats. Intense protein carbonyl immunoreactivity was localized in cell bodies. Our study suggests that increased protein oxidation may be an important part of the mechanism of Tat neurotoxicity. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.