The involvement of ethanol in the free radical reaction of 6-hydroxydopamine.
The involvement of ethanol in the free radical reaction of 6-hydroxydopamine.
复制标题
乙醇参与 6-羟基多巴胺的自由基反应。
DOI：
10.1007/bf00965833
复制
发表时间：
1991
影响因子：
4.4
通讯作者：
Sun,AY
中科院分区：
文献类型：
--
作者：
Oldfield,FF;Cowan,DL;Sun,AY
ESR自旋捕集技术用于检测和分析自由基的形成。当6-羟基多巴胺（6-OHDA）单独孵育或与自由基产生系统（H2 O2和FeSO 4）共同孵育时，可观察到浓度依赖性的羟基自由基。与维生素E或甘露醇相比，谷氨酸是ESR信号最有效的清除剂。乙醇的加入导致纯羟乙基自由基的形成。羟乙基自由基的生成量与乙醇浓度有关，羟乙基自由基的生成与脂质过氧化程度和膜结合（Na+，K+）-ATP酶活性的丧失密切相关。我们认为，在生物系统中，乙醇可能会增强6-OHDA的神经毒性，形成羟乙基自由基，这是更长的寿命和更大的损害膜的羟基自由基。这些数据使我们进一步假设，由6-OHDA和其他产生自由基的化合物引起的神经元变性可以在乙醇存在下增强。
ESR spin trapping technique was used to detect and analyze free radical formation. When 6-hydroxydomine (6-OHDA) was incubated alone or in the presence of a free radical generating system (H2O2and FeSO4), hydroxyl free radicals were observed in a concentration-dependent manner. Glutathione was found to be the most effective scavenger of the ESR signal when compared with vitamin E or Mannitol. The addition of ethanol resulted in the formation of the pure hydroxyethyl free radicals. The amount of hydroxyethyl free radicals in the system was dependent upon the concentration of ethanol and the formation of hydroxyethyl free radicals correlated well with the extent of lipid peroxidation and the loss of enzymic activity of the membrane-bound (Na+, K+)-ATPase. We suggest that in the biological system ethanol may potentiate the neurotoxicity of 6-OHDA with the formation of hydroxyethyl free radicals, which are longer-lived and far more damaging to membranes that the hydroxyl radicals. These data lead us to further hypothesize that the neuronal degeneration caused by 6-OHDA and other compounds that generate free radicals could be potentiated in the presence of ethanol.