期刊
JOURNAL OF NEUROCHEMISTRY
卷 123, 期 5, 页码 824-836出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1471-4159.2012.07888.x
关键词
brain; Golgi complex; apparatus; manganese; primary cell culture; SPCA; toxicity
资金
- Programa de Incorporacion de Doctores, Junta de Extremadura (Spain)
- MICINN [BFU2011-23313]
- Fundacion Marcelino Botin
- Junta de Extremadura
- FEDER
Excess Mn2+ in humans causes a neurological disorder known as manganism, which shares symptoms with Parkinson's disease. However, the cellular mechanisms underlying Mn2+-neurotoxicity and the involvement of Mn2+-transporters in cellular homeostasis and repair are poorly understood and require further investigation. In this work, we have analyzed the effect of Mn2+ on neurons and glia from mice in primary cultures. Mn2+ overload compromised survival of both cell types, specifically affecting cellular integrity and Golgi organization, where the secretory pathway Ca2+/Mn2+-ATPase is localized. This ATP-driven Mn2+ transporter might take part in Mn2+ accumulation/detoxification at low loads of Mn2+, but its ATPase activity is inhibited at high concentration of Mn2+. Glial cells appear to be significantly more resistant to this toxicity than neurons and their presence in cocultures provided some protection to neurons against degeneration induced by Mn2+. Interestingly, the Mn2+ toxicity was partially reversed upon Mn2+ removal by wash out or by the addition of EDTA as a chelating agent, in particular in glial cells. These studies provide data on Mn2+ neurotoxicity and may contribute to explore new therapeutic approaches for reducing Mn2+ poisoning.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据