Tohgi H, Abe T, Yamazaki K, Murata T, Ishizaki E, Isobe C
Department of Neurology, Iwate Medical University, Morioka, Japan.
Neurosci Lett. 1999 Feb 5;260(3):204-6. doi: 10.1016/s0304-3940(98)00986-0.
To determine the role of free radical mechanisms in the pathogenesis of amyotrophic lateral sclerosis (ALS), cerebrospinal fluid concentrations of oxidized nitric oxide (NO) products (nitrite and nitrate) and reduced and oxidized forms of glutathione (GSH and GSSG, respectively) were compared between patients with the sporadic form of ALS (SALS) and controls. In the SALS patients, the nitrate levels were significantly higher (by 73%) in contrast to remarkably lower GSSG/GSH ratio, approximately 3-fold, compared to controls. These results suggest that NO production or oxidation is activated in SALS patients, leading to a decrease in superoxide radicals to oxidize GSH. The subsequent generation of a highly reactive anion, peroxynitrite, may play a causal role in the pathogenesis of SALS.
为了确定自由基机制在肌萎缩侧索硬化症（ALS）发病机制中的作用，比较了散发性ALS（SALS）患者和对照组脑脊液中氧化型一氧化氮（NO）产物（亚硝酸盐和硝酸盐）以及还原型和氧化型谷胱甘肽（分别为GSH和GSSG）的浓度。在SALS患者中，硝酸盐水平显著升高（升高73%），而与对照组相比，GSSG/GSH比值显著降低，约为对照组的三分之一。这些结果表明，SALS患者中NO的产生或氧化被激活，导致超氧自由基减少，从而氧化GSH。随后产生的高反应性阴离子过氧亚硝酸盐可能在SALS的发病机制中起因果作用。
