Graham D G
Neurotoxicology. 1984 Spring;5(1):83-95.
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.
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。