Beal M Flint
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, NY 10021, USA.
Free Radic Biol Med. 2002 May 1;32(9):797-803. doi: 10.1016/s0891-5849(02)00780-3.
There is a large body of evidence implicating oxidative damage in the pathogenesis of both normal aging and neurodegenerative diseases. Oxidative damage to proteins has been well established. Although there are a large number of potential oxidative modifications only a few have been systematically studied. The most frequently studied marker of oxidative damage to proteins is protein carbonyl groups. 3-Nitrotyrosine is thought to be a relatively specific marker of oxidative damage mediated by peroxynitrite. Increased concentrations of both protein carbonyls and 3-nitrotyrosine have been documented in both normal aging as well as in Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). These findings help to provide a rationale for trials of antioxidants in neurodegenerative diseases.
有大量证据表明氧化损伤与正常衰老和神经退行性疾病的发病机制有关。蛋白质的氧化损伤已得到充分证实。虽然存在大量潜在的氧化修饰，但只有少数被系统研究过。蛋白质氧化损伤最常研究的标志物是蛋白质羰基。3-硝基酪氨酸被认为是过氧亚硝酸盐介导的氧化损伤的相对特异性标志物。在正常衰老以及阿尔茨海默病（AD）、帕金森病（PD）和肌萎缩侧索硬化症（ALS）中，蛋白质羰基和3-硝基酪氨酸的浓度均有所增加。这些发现有助于为神经退行性疾病的抗氧化剂试验提供理论依据。
