Pamplona Reinald, Ilieva Ekaterina, Ayala Victoria, Bellmunt Maria Josep, Cacabelos Daniel, Dalfo Esther, Ferrer Isidre, Portero-Otin Manuel
Department of Experimental Medicine, School of Medicine, University of Lleida-IRBLLEIDA, Lleida 25008, Spain.
Ann N Y Acad Sci. 2008 Apr;1126:315-9. doi: 10.1196/annals.1433.014. Epub 2007 Dec 13.
Nonenzymatic protein modifications are generated from direct oxidation of amino acid side chains and from reaction of the nucleophilic side chains of specific amino acids with reactive carbonyl species. These reactions give rise to specific markers that have been analyzed in different neurodegenerative diseases sharing protein aggregation, such as Alzheimer's disease, Pick's disease, Parkinson's disease, dementia with Lewy bodies, Creutzfeldt-Jakob disease, and amyotrophic lateral sclerosis. Collectively, available data demonstrate that oxidative stress homeostasis, mitochondrial function, and energy metabolism are key factors in determining the disease-specific pattern of protein molecular damage. In addition, these findings suggest the lack of a "gold marker of oxidative stress," and, consequently, they strengthen the need for a molecular dissection of the nonenzymatic reactions underlying neurodegenerative processes.
非酶蛋白修饰源于氨基酸侧链的直接氧化以及特定氨基酸的亲核侧链与活性羰基物质的反应。这些反应产生了特定的标志物，已在患有蛋白质聚集的不同神经退行性疾病中进行了分析，如阿尔茨海默病、皮克病、帕金森病、路易体痴呆、克雅氏病和肌萎缩侧索硬化症。总体而言，现有数据表明氧化应激稳态、线粒体功能和能量代谢是决定蛋白质分子损伤疾病特异性模式的关键因素。此外，这些发现表明缺乏“氧化应激的金标准标志物”，因此，它们强化了对神经退行性过程中非酶反应进行分子剖析的必要性。
