Neurology Department, Hôpital A. Michallon, Grenoble, France.
Neurochem Res. 2010 Oct;35(10):1530-7. doi: 10.1007/s11064-010-0212-5. Epub 2010 Jun 10.
We examined oxidative stress markers of 31 patients suffering from ALS, 24 patients suffering from PD and 30 healthy subjects were included. We determined the plasma levels of lipid peroxidation (malondialdehyde, MDA), of protein oxidative lesions (plasma glutathione, carbonyls and thiols) and the activity of antioxidant enzymes i.e. erythrocyte Cu,Zn-Superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and catalase. MDA and thiols were significantly different in both neurodegenerative diseases versus control population. A trend for an enhancement of oxidized glutathione was noted in ALS patients. Univariate analysis showed that SOD activity was significantly decreased in ALS and GSH-Px activity was decreased in PD. After adjusting for demographic parameters and enzyme cofactors, we could emphasize a compensatory increase of SOD activity in PD. Different antioxidant systems were not involved in the same way in ALS and PD, suggesting that oxidative stress may be a cause rather than a consequence of the neuronal death.
我们检测了 31 名肌萎缩侧索硬化症（ALS）患者、24 名帕金森病（PD）患者和 30 名健康对照者的氧化应激标志物。我们测定了血浆丙二醛（MDA）、蛋白氧化损伤（血浆谷胱甘肽、羰基和巯基）和抗氧化酶的活性，如红细胞 Cu，Zn-超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶。MDA 和巯基在两种神经退行性疾病与对照组之间存在显著差异。ALS 患者的氧化型谷胱甘肽呈升高趋势。单因素分析显示，ALS 患者的 SOD 活性显著降低，PD 患者的 GSH-Px 活性降低。在调整了人口统计学参数和酶辅助因子后，我们可以强调 PD 中 SOD 活性的代偿性增加。不同的抗氧化系统在 ALS 和 PD 中的参与方式不同，这表明氧化应激可能是神经元死亡的原因，而不是结果。
