Department of Pharmacology and Physiology, Universidad de Zaragoza, Spain.
J Bioenerg Biomembr. 2011 Apr;43(2):181-6. doi: 10.1007/s10863-011-9348-5. Epub 2011 Mar 31.
A mutant form of the copper/zinc superoxide dismutase (SOD1) protein is found in some patients with amyotrophic lateral sclerosis (ALS). Alteration of the activity of this antioxidant enzyme leads to an oxidative stress imbalance, which damages the structure of lipids and proteins in the CNS. Using fluorescence spectroscopy, we monitored membrane fluidity in the spinal cord and the brain in a widely used animal model of ALS, the SOD(G93A) mouse, which develops symptoms similar to ALS with an accelerated course. Our results show that the membrane fluidity of the spinal cord in this animal model significantly decreased in symptomatic animals compared with age-matched littermate controls. To the best of our knowledge, this is the first report showing that membrane fluidity is affected in the spinal cord of a SOD(G93A) animal model of ALS. Changes in membrane fluidity likely contribute substantially to alterations in cell membrane functions in the nervous tissue from SOD(G93A) mice.
一种突变形式的铜/锌超氧化物歧化酶（SOD1）蛋白存在于一些肌萎缩侧索硬化症（ALS）患者中。这种抗氧化酶活性的改变导致氧化应激失衡，从而破坏中枢神经系统中脂质和蛋白质的结构。我们使用荧光光谱法监测了在一种广泛应用的 ALS 动物模型（SOD(G93A) 小鼠）中脊髓和大脑的膜流动性，该模型具有与 ALS 相似的加速病程的症状。我们的结果表明，与年龄匹配的同窝对照相比，该动物模型中症状性动物的脊髓膜流动性显著降低。据我们所知，这是首次报道表明 SOD(G93A) ALS 动物模型的脊髓膜流动性受到影响。膜流动性的变化可能会极大地影响 SOD(G93A) 小鼠神经组织中细胞膜功能的改变。
