IRON, SELENIUM AND GLUTATHIONE-PEROXIDASE ACTIVITY ARE ELEVATED IN SPORADIC MOTOR-NEURON DISEASE

被引：80

作者：

INCE, PG

SHAW, PJ

CANDY, JM

MANTLE, D

TANDON, L

EHMANN, WD

MARKESBERY, WR

机构：

[1] UNIV NEWCASTLE UPON TYNE,DIV CLIN NEUROSCI,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND

[2] UNIV NEWCASTLE UPON TYNE,DIV NEUROBIOL,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND

[3] UNIV KENTUCKY,SANDERS BROWN CTR AGING,LEXINGTON,KY

来源：

NEUROSCIENCE LETTERS | 1994年 / 182卷 / 01期

基金：

英国惠康基金;

关键词：

IRON; SELENIUM; MOTOR NEURON DISEASE; GLUTATHIONE PEROXIDASE; FREE RADICAL; NEURODEGENERATIVE DISEASE; SUPEROXIDE DISMUTASE;

D O I：

10.1016/0304-3940(94)90213-5

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Oxygen free radical damage is strongly implicated in the pathogenesis of familial motor neuron disease (MND) associated with mutation of the Cu/Zn superoxide dismutase gene, and may be relevant in sporadic MND. Selenium (Se) and iron (Fe) have important roles in free radical metabolism. Using neutron activation analysis we have demonstrated significant elevation of Se and Fe in lumbar spinal cord in MND cases (38) compared to controls (22). Analysis of enzymes involved in free radical scavenging showed a significant and specific increase in the activity of the selenoprotein enzyme glutathione peroxidase in MND spinal cord.

引用

页码：87 / 90

页数：4

共 17 条

[1] SUPEROXIDE-DISMUTASE ACTIVITY, OXIDATIVE DAMAGE, AND MITOCHONDRIAL ENERGY-METABOLISM IN FAMILIAL AND SPORADIC AMYOTROPHIC-LATERAL-SCLEROSIS [J].