Department of Neurology, Medical University in Warsaw, ul. Kondratowicza 8, 03-242 Poland.
Parkinsonism Relat Disord. 2011 Jul;17(6):423-30. doi: 10.1016/j.parkreldis.2011.03.016. Epub 2011 May 7.
Oxidative stress is considered one of the pathways leading to neuronal death in neurodegenerative disease. Many published studies aimed to assess the possible role of iron in this process but no consensus has been reached. On the other hand little is known about the role played by the main iron storage protein - ferritin. In this review we discuss the data obtained using several methods - Mössbauer spectroscopy, electron microscopy and ELISA - from human brain tissue both in controls and in four neurodegenerative disorders - Parkinson's (PD) and Alzheimer's disease, progressive supranuclear palsy and neuroferritinopathy. Iron may only cause oxidative stress injury when it is available as labile iron for Fenton reaction. This may be related to the decreased ability of ferritin to retain iron within the iron core of ferritin. This happens in PD and in neuroferritinopathy. In PD there is a decrease in the concentration of L ferritin, while in neuroferritinopathy there is a genetically induced mutation in L ferritin causing its loss of function. We discuss the importance of the ratio H/L ferritin and its changes in neurodegeneration.
氧化应激被认为是导致神经退行性疾病神经元死亡的途径之一。许多已发表的研究旨在评估铁在这一过程中的可能作用，但尚未达成共识。另一方面，人们对主要的铁储存蛋白——铁蛋白所扮演的角色知之甚少。在这篇综述中，我们讨论了使用几种方法——穆斯堡尔光谱学、电子显微镜和 ELISA——从对照组和四种神经退行性疾病（帕金森病和阿尔茨海默病、进行性核上性麻痹和神经铁蛋白病）的人脑组织中获得的数据。只有当铁作为芬顿反应的不稳定铁可用时，铁才会引起氧化应激损伤。这可能与铁蛋白保留铁在铁蛋白铁核心内的能力下降有关。这种情况发生在帕金森病和神经铁蛋白病中。在帕金森病中，L 铁蛋白的浓度降低，而在神经铁蛋白病中，L 铁蛋白发生了遗传诱导突变，导致其功能丧失。我们讨论了 H/L 铁蛋白比值及其在神经退行性变中的变化的重要性。
