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铁在神经退行性变中的作用——穆斯堡尔光谱学、电子显微镜、酶联免疫吸附测定和神经影像学研究。

The role of iron in neurodegeneration--Mössbauer spectroscopy, electron microscopy, enzyme-linked immunosorbent assay and neuroimaging studies.

机构信息

Faculty of Physics, Warsaw University of Technology, Warsaw, Poland.

出版信息

J Phys Condens Matter. 2012 Jun 20;24(24):244106. doi: 10.1088/0953-8984/24/24/244106. Epub 2012 May 18.

DOI:10.1088/0953-8984/24/24/244106
PMID:22595616
Abstract

The possible role of iron in neurodegeneration was studied by various techniques: electron microscopy, enzyme-linked immunosorbent assay, Mössbauer spectroscopy, atomic absorption, ultrasonography and magnetic resonance imaging. The measurements were made on human tissues extracted from liver and from brain structures involved in diseases of the human brain: substantia nigra (Parkinson's, PD), hippocampal cortex (Alzheimer's, AD) and globus pallidus (progressive supranuclear palsy, PSP). The sizes of the iron cores of ferritin, the main iron storage compound in tissues, were found to be smaller in brain than in liver. Brain ferritin has a higher proportion of H to L chains compared to liver. A significant decrease of the concentration of L chains in PD compared to control was found. No increase in the concentration of iron in PD versus control was detected; however, there was an increase of labile iron, which constitutes only 2‰ of brain iron. In AD an increase in the concentration of ferritin was noticed, without a significant increase in iron concentration. In PSP an increase of total iron was observed. Our findings suggest that the mechanisms leading to the death of nerve cells in these three diseases may be different, although all may be related to iron mediated oxidative stress.

摘要

铁在神经退行性变中的可能作用已通过各种技术进行了研究

电子显微镜、酶联免疫吸附测定、穆斯堡尔光谱学、原子吸收、超声和磁共振成像。这些测量是在从肝脏和涉及人脑疾病的脑结构中提取的人体组织上进行的:黑质(帕金森病,PD)、海马皮层(阿尔茨海默病,AD)和苍白球(进行性核上性麻痹,PSP)。发现组织中铁蛋白(主要的铁储存化合物)的铁核大小在脑内比在肝内小。脑铁蛋白的 H 链与 L 链的比例高于肝铁蛋白。与对照组相比,PD 中 L 链的浓度显著降低。在 PD 与对照组相比,未检测到铁浓度增加;然而,有不稳定铁的增加,其仅占脑铁的 2‰。在 AD 中,注意到铁蛋白浓度增加,而铁浓度没有显著增加。在 PSP 中观察到总铁增加。我们的发现表明,尽管所有这些疾病可能都与铁介导的氧化应激有关,但导致这三种疾病中神经细胞死亡的机制可能不同。

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