Creutzfeldt-Jakob disease and oxidative stress

被引:16
作者
Bleich, S
Kropp, S
Degner, D
Zerr, I
Pilz, J
Gleiter, CH
Otto, M
Rüther, E
Kretzschmar, HA
Wiltfang, J
Kornhuber, J
Poser, S
机构
[1] Univ Gottingen, Dept Psychiat, D-37075 Gottingen, Germany
[2] Univ Gottingen, Dept Neurol, D-37075 Gottingen, Germany
[3] Univ Gottingen, Dept Clin Pharmacol, D-37075 Gottingen, Germany
[4] Univ Gottingen, Dept Neuropathol, D-37075 Gottingen, Germany
来源
ACTA NEUROLOGICA SCANDINAVICA | 2000年 / 101卷 / 05期
关键词
Creutzfeldt-Jakob disease; malondialdehyde; lipid peroxidation; oxidative stress;
D O I
10.1034/j.1600-0404.2000.9s290a.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objectives - Substantial evidence supports the hypothesis that oxygen free radicals are involved in various neurodegenerative disorders. To assess the presence of oxidative stress in Creutzfeldt-Jakob disease (CJD) we examined the concentrations of malondialdehyde (MDA) as an established marker of lipid peroxidation. Material and methods - MDA was quantified by high performance liquid chromatography (HPLC) in cerebrospinal fluid (CSF; n=12) and in serum (n=11) samples of CJD patients and healthy controls (n=15). Results - Mean values in healthy controls: 2.56 nmol/ml +/- 0.46 (CSF) and 1.94 nmol/ml +/- 0.67 (serum); mean values in CJD patients: 2.64 nmol/ml +/- 0.67 (CSF) and 1.68 nmol/ml +/- 0.79 (serum). No significant (P > 0.05) difference between CJD patients and controls was observed. Conclusions - The results indicated that the CSF and serum of CJD patients showed no higher endogenous levels of MDA as compared to normal healthy controls. These findings provide no evidence for an additional role of oxidative stress in the pathogenetic mechanism underlying CJD neurodegeneration.
引用
收藏
页码:332 / 334
页数:3
相关论文
共 12 条
[1]   HUMAN SPONGIFORM ENCEPHALOPATHY - THE NATIONAL-INSTITUTES-OF-HEALTH SERIES OF 300 CASES OF EXPERIMENTALLY TRANSMITTED DISEASE [J].
BROWN, P ;
GIBBS, CJ ;
RODGERSJOHNSON, P ;
ASHER, DM ;
SULIMA, MP ;
BACOTE, A ;
GOLDFARB, LG ;
GAJDUSEK, DC .
ANNALS OF NEUROLOGY, 1994, 35 (05) :513-529
[2]   CHEMISTRY AND BIOCHEMISTRY OF 4-HYDROXYNONENAL, MALONALDEHYDE AND RELATED ALDEHYDES [J].
ESTERBAUER, H ;
SCHAUR, RJ ;
ZOLLNER, H .
FREE RADICAL BIOLOGY AND MEDICINE, 1991, 11 (01) :81-128
[3]  
Esterbauer H, 1996, PATHOL BIOL, V44, P25
[4]  
Floyd R.A., 1992, Ann. Neurol, V32, P22
[5]   OXYGEN-TOXICITY, OXYGEN RADICALS, TRANSITION-METALS AND DISEASE [J].
HALLIWELL, B ;
GUTTERIDGE, JMC .
BIOCHEMICAL JOURNAL, 1984, 219 (01) :1-14
[6]   LIPID-PEROXIDATION AND FREE-RADICAL SCAVENGERS IN ALZHEIMERS-DISEASE [J].
JEANDEL, C ;
NICOLAS, MB ;
DUBOIS, F ;
NABETBELLEVILLE, F ;
PENIN, F ;
CUNY, G .
GERONTOLOGY, 1989, 35 (5-6) :275-282
[7]  
PILZ J, UNPUB J CHROMATOGR
[8]   ALZHEIMER-DISEASE AND THE PRION DISORDERS AMYLOID BETA-PROTEIN AND PRION PROTEIN AMYLOIDOSES [J].
PRICE, DL ;
BORCHELT, DR ;
SISODIA, SS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (14) :6381-6384
[9]   HUMAN PRION DISEASES [J].
PRUSINER, SB ;
HSIAO, KK .
ANNALS OF NEUROLOGY, 1994, 35 (04) :385-395
[10]  
PRYOR WA, 1994, NATURAL ANTIOXIDANTS