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家族性和散发性肌萎缩侧索硬化症中铜/锌超氧化物歧化酶活性

Cu/Zn superoxide dismutase activity in familial and sporadic amyotrophic lateral sclerosis.

作者信息

Robberecht W, Sapp P, Viaene M K, Rosen D, McKenna-Yasek D, Haines J, Horvitz R, Theys P, Brown R

机构信息

Department of Neurology, University Hospital Gasthuisberg, Leuven, Belgium.

出版信息

J Neurochem. 1994 Jan;62(1):384-7. doi: 10.1046/j.1471-4159.1994.62010384.x.

Abstract

Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron disease that is inherited as an autosomal dominant trait in approximately 10% of cases. Recently we and others identified several single-base mutations in the Cu/Zn superoxide dismutase (SOD1) gene in patients with familial ALS (FALS). Using single-strand conformational polymorphism, we studied the C to G mutation in exon 2 of the SOD1 gene (resulting in a leucine to valine substitution in position 38) in affected and unaffected members of a large Belgian family with FALS. We measured the SOD1 activity in red blood cell lysates in 14 members of this family, including the only surviving clinically affected patient. SOD1 activity of the family members carrying the mutation was less than half that of members without the mutation. In addition, in 11 patients with sporadic ALS and 11 age- and sex-matched controls, red blood cell SOD1 activity was normal. These studies indicate that SOD1 activity is reduced in these FALS patients but not in sporadic ALS patients. Moreover, this SOD1 enzyme abnormality is detectable years before onset of clinical ALS in carriers of this FALS mutation.

摘要

肌萎缩侧索硬化症(ALS)是一种退行性运动神经元疾病,约10%的病例呈常染色体显性遗传。最近,我们及其他研究人员在家族性ALS(FALS)患者的铜/锌超氧化物歧化酶(SOD1)基因中发现了几个单碱基突变。我们利用单链构象多态性,研究了一个患有FALS的比利时大家庭中患病和未患病成员的SOD1基因外显子2中C到G的突变(导致第38位的亮氨酸被缬氨酸取代)。我们检测了这个家族14名成员红细胞裂解物中的SOD1活性,其中包括唯一存活的临床患病患者。携带该突变的家族成员的SOD1活性不到未携带突变成员的一半。此外,在11例散发性ALS患者和11例年龄及性别匹配的对照中,红细胞SOD1活性正常。这些研究表明,这些FALS患者的SOD1活性降低,但散发性ALS患者中未降低。此外,在携带这种FALS突变的个体中,在临床ALS发病前数年就能检测到这种SOD1酶异常。

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