Department of Pharmaceutical Sciences, Northeastern University, 360 Huntington Avenue 148TF, Boston, MA 02115, USA.
Metallomics. 2017 Aug 16;9(8):1028-1046. doi: 10.1039/c7mt00079k.
Although manganese (Mn) is critical for the proper functioning of various metabolic enzymes and cofactors, excess Mn in the brain causes neurotoxicity. While the exact transport mechanism of Mn has not been fully understood, several importers and exporters for Mn have been identified over the past decade. In addition to Mn-specific transporters, it has been demonstrated that iron transporters can mediate Mn transport in the brain and peripheral tissues. However, while the expression of iron transporters is regulated by body iron stores, whether or not disorders of iron metabolism modify Mn homeostasis has not been systematically discussed. The present review will provide an update on the role of altered iron status in the transport and toxicity of Mn.
虽然锰（Mn）对各种代谢酶和辅助因子的正常功能至关重要，但大脑中过量的 Mn 会导致神经毒性。尽管 Mn 的确切转运机制尚未完全了解，但在过去十年中已经确定了几种 Mn 的进口器和出口器。除了 Mn 特异性转运蛋白外，还已经证明铁转运蛋白可以介导脑和外周组织中的 Mn 转运。然而，尽管铁转运蛋白的表达受体内铁储存的调节，但铁代谢紊乱是否会改变 Mn 稳态尚未得到系统讨论。本综述将提供有关铁状态改变在 Mn 转运和毒性中的作用的最新信息。
