Pelizzoni Ilaria, Macco Romina, Zacchetti Daniele, Grohovaz Fabio, Codazzi Franca
San Raffaele Scientific Institute, Milan, Italy.
Biochem Soc Trans. 2008 Dec;36(Pt 6):1309-12. doi: 10.1042/BST0361309.
Iron and calcium are required for general cellular functions, as well as for specific neuronal-related activities. However, a pathological increase in their levels favours oxidative stress and mitochondrial damage, leading to neuronal death. Neurodegeneration can thus be determined by alterations in ionic homoeostasis and/or pro-oxidative-antioxidative equilibrium, two conditions that vary significantly in different kinds of brain cell and also with aging. In the present review, we re-evaluate recent data on NTBI (non-transferrin bound iron) uptake that suggest a strict interplay with the mechanisms of calcium control. In particular, we focus on the use of common entry pathways and on the way cytosolic calcium can modulate iron entry and determine its intracellular accumulation.
铁和钙是细胞正常功能以及特定神经元相关活动所必需的。然而，它们水平的病理性升高会促进氧化应激和线粒体损伤，导致神经元死亡。因此，神经退行性变可由离子稳态和/或促氧化-抗氧化平衡的改变来决定，这两种情况在不同类型的脑细胞中以及随着年龄增长会有显著差异。在本综述中，我们重新评估了关于非转铁蛋白结合铁（NTBI）摄取的最新数据，这些数据表明其与钙调控机制存在紧密的相互作用。特别是，我们关注共同的进入途径的使用以及胞质钙调节铁进入并决定其细胞内积累的方式。
