Suppr超能文献

儿茶酚胺毒性:锰神经毒性和帕金森病分子发病机制的一种假说

Catecholamine toxicity: a proposal for the molecular pathogenesis of manganese neurotoxicity and Parkinson's disease.

作者信息

Graham D G

出版信息

Neurotoxicology. 1984 Spring;5(1):83-95.

PMID:6538951
Abstract

An hypothesis is presented which attempts to relate the pathogenesis of both manganese neurotoxicity and Parkinson's disease to cytotoxicity from products of catecholamine oxidation. These include the products resulting from the partial reduction of oxygen (superoxide anion, hydroxyl radical, and hydrogen peroxide) and the semiquinones and ortho quinones produced during autoxidation or oxidation of catecholamines initiated by trivalent manganese.

摘要

本文提出了一种假说,试图将锰神经毒性和帕金森病的发病机制与儿茶酚胺氧化产物的细胞毒性联系起来。这些产物包括部分还原氧产生的物质(超氧阴离子、羟基自由基和过氧化氢)以及由三价锰引发的儿茶酚胺自氧化或氧化过程中产生的半醌和邻醌。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验