Mecocci P, Polidori M C, Ingegni T, Cherubini A, Chionne F, Cecchetti R, Senin U
Institute of Gerontology and Geriatrics, University of Perugia, Italy.
Neurology. 1998 Oct;51(4):1014-7. doi: 10.1212/wnl.51.4.1014.
Several studies show structural and functional alterations in peripheral cells in AD. The purpose of this study was to evaluate oxidative stress in AD lymphocytes.
The literature supports the role of reactive oxygen species in the pathogenesis of AD because several markers of oxidative damage have been detected in AD brain.
8-hydroxy-2'-deoxyguanosine (8OHdG), a marker of oxidative stress in DNA, was measured in lymphocytes of AD patients and healthy aged controls with high-pressure liquid chromatography with electrochemical detection, both at basal condition and after acute oxidative stress with hydrogen peroxide.
A significantly higher concentration of 8OHdG in lymphocytes occurred in AD patients compared with controls. In this latter group, 8OHdG increased progressively with age. After acute oxidative stress, levels of formed 8OHdG did not differ between AD patients and controls.
Our results support that AD is affected by oxidative stress, detectable not only in the brain but also in peripheral cells; oxidative mechanisms may contribute to the pathogenesis of AD. Additional studies in other neurodegenerative diseases are needed to evaluate these findings.
多项研究表明，阿尔茨海默病（AD）患者外周细胞存在结构和功能改变。本研究旨在评估AD患者淋巴细胞中的氧化应激。
文献支持活性氧在AD发病机制中的作用，因为在AD大脑中已检测到多种氧化损伤标志物。
采用高压液相色谱电化学检测法，在基础状态及用过氧化氢进行急性氧化应激后，检测AD患者和健康老年对照者淋巴细胞中DNA氧化应激标志物8-羟基-2'-脱氧鸟苷（8OHdG）的水平。
与对照组相比，AD患者淋巴细胞中8OHdG浓度显著更高。在对照组中，8OHdG水平随年龄增长而逐渐升高。急性氧化应激后，AD患者和对照组中生成的8OHdG水平无差异。
我们的结果支持AD受氧化应激影响，不仅在大脑中可检测到，在外周细胞中也可检测到；氧化机制可能参与AD的发病过程。需要在其他神经退行性疾病中进行更多研究以评估这些发现。
