Cohen O, Kohen R, Lavon E, Abramsky O, Steiner I
Department of Neurology, Hadassah University Hospital, Hebrew University Hadassah Medical School, Jerusalem, Israel.
J Neurol Sci. 1996 Nov;143(1-2):118-20. doi: 10.1016/s0022-510x(96)00190-6.
Accumulated evidence implies that mutations in the gene coding for Cu/Zn superoxide dismutase (SOD) are associated with the pathogenesis of the familial form of amyotrophic lateral sclerosis (ALS). The clinical and pathological similarities of the familial and the sporadic forms of the disease may suggest that abnormal SOD activity takes also part in the pathogenesis of sporadic ALS. We therefore measured serum SOD activity in fifteen sporadic ALS patients. Mean serum SOD activity was 1.15 +/- 0.40 u/ml in ALS patients, 1.50 +/- 0.45 u/ml. in patients with other neurological disorders and 1.45 +/- 0.45 u/ml in.healthy controls (p < 0.021 and p < 0.031 respectively). If this sporadic ALS-related reduction in serum SOD activity will be confirmed in the diseased nervous system tissue, it may suggest that abnormal SOD activity is also associated with the motor neuron damage in the sporadic form of ALS.
越来越多的证据表明，编码铜/锌超氧化物歧化酶（SOD）的基因突变与家族性肌萎缩侧索硬化症（ALS）的发病机制有关。该疾病家族性和散发性形式在临床和病理上的相似性可能表明，超氧化物歧化酶活性异常也参与了散发性ALS的发病机制。因此，我们测量了15例散发性ALS患者的血清超氧化物歧化酶活性。ALS患者的平均血清超氧化物歧化酶活性为1.15±0.40u/ml，其他神经系统疾病患者为1.50±0.45u/ml，健康对照者为1.45±0.45u/ml（p分别<0.021和p<0.031）。如果散发性ALS相关的血清超氧化物歧化酶活性降低在患病神经系统组织中得到证实，则可能表明超氧化物歧化酶活性异常也与散发性ALS形式中的运动神经元损伤有关。
