Manganese transport and Na/K/Cl cotransport in PC-12 cells.
Manganese transport and Na/K/Cl cotransport in PC-12 cells.
复制标题
PC-12 细胞中的锰转运和 Na/K/Cl 共转运。
DOI：
10.1111/j.1749-6632.1993.tb18325.x
复制
发表时间：
1993
影响因子：
5.2
通讯作者：
Sun,AY
中科院分区：
文献类型：
--
作者：
Kim,HD;Sun,GY;Sun,AY
锰是一种必需的微量金属，可被消化道吸收和排出。锰以微量存在于大脑的各个区域。众所周知，锰缺乏症虽然在人类中很少见，但会增强癫痫发作的易感性。“在许多物种中，产后期间缺乏锰会引发先天性不可逆转的共济失调。2与此相反，锰的毒性已被广泛研究。早期锰中毒的最初损害似乎是由神经递质代谢的生化缺陷引起的，包括多巴胺、血清素和γ-氨基-正丁酸。s3随着锰中毒的进展，组织病理学病变，不像帕金森病，出现在大脑中，导致永久性神经系统疾病。2-3锰通过一个可饱和的过程穿过血脑屏障，星形胶质细胞也通过一种特异性的高亲和力转运来摄取锰。锰的组织分布的一个有趣的特征是，神经胶质细胞而不是神经元细胞富集锰，其数量级高于简单的被动锡永。在细胞内的细胞器中，线粒体是储存锰的主要场所。在这篇文章中，我们报告了我们对锰进入PC-12细胞的机制的调查结果，以及随后的intracel-Mar锰对其他离子转运过程的影响。
Manganese is an essential trace metal which is both absorbed and excreted by the alimentary tract. Manganese is present in minute amounts in various regions of the brain. It is known that manganese deficiency, while rare in humans, enhances the susceptibility to seizures.'In a number of species, manganese deficiency during the postnatal period elicits a congenital irreversible ataxia. 2 By contrast, manganese toxicity has been extensively d~ cumented.~.~ The initial damage in early manganese toxicity appears to result from a biochemical defect in the metabolism of neurotransmitters, including dopamine, serotonin, and y-amino-n-butyric acid.* s3 With progression of manganese toxicity, histopathological lesions, not unlike those of Parkinson's disease, appear in the brain, causing a permanent neurological disorder. 2-3Manganese is transported across the blood-brain barrier by a saturable process., Astrocytes also take up manganese by a specific high affinity transport~ ystem.~ An interesting feature of the tissue distribution of manganese is that glial cells, but not neuronal cells, concentrate manganese an order of magnitude higher than can be accounted for by a simple passive diff~ sion.~ Of the intracellular organelles, mitochondria are the primary site within which manganese is stored.* In this communication, we report the results of our investigation on the mechanism by which manganese enters PC-12 cells, and the subsequent effects of intracel-Mar manganese on other ion transport processes.