Influence of vitamin E and C supplementation on lipoprotein oxidation in patients with Alzheimer's disease

被引:97
作者
Kontush, A
Mann, U
Arlt, S
Ujeyl, A
Lührs, C
Müller-Thomsen, T
Beisiegel, U
机构
[1] Univ Hamburg, Hosp Eppendorf, Psychiat Clin, D-20246 Hamburg, Germany
[2] Univ Hamburg, Hosp Eppendorf, Med Clin, D-20246 Hamburg, Germany
关键词
Alzheimer's disease; oxidation; vitamin E; vitamin C; lipoproteins; cerebrospinal fluid; plasma; antioxidants; free radicals;
D O I
10.1016/S0891-5849(01)00595-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Because increased oxidation is an important feature of Alzheimer's disease (AD) and low concentrations of antioxidant vitamins C and E have been observed in cerebrospinal fluid (CSF) of AD patients, supplementation with these antioxidants might delay the development of AD. Major targets for oxidation in brain are lipids and lipoproteins. We studied whether supplementation with antioxidative vitamins E and C can increase their concentrations not only in plasma but also in CSF, and as a consequence decrease the susceptibility of lipoproteins to in vitro oxidation. Two groups, each consisting of 10 patients with AD, were for I month supplemented daily with either a combination of 400 IU vitamin E and 1000 mg vitamin C, or 400 IU vitamin E alone. We found that supplementation with vitamin E and C significantly increased the concentrations of both vitamins in plasma and CSF. Importantly, the abnormally low concentrations of vitamin C were returned to normal level following treatment. As a consequence, susceptibility of CSF and plasma lipoproteins to in vitro oxidation was significantly decreased. In contrast, the supplementation with vitamin E alone significantly increased its CSF and plasma concentrations, but was unable to decrease the lipoprotein oxidizability. These findings document a superiority of a combined vitamin E + C supplementation over a vitamin E supplementation alone in AD and provide a biochemical basis for its use. (C) 2001 Elsevier Science Inc.
引用
收藏
页码:345 / 354
页数:10
相关论文
共 50 条
[1]   Time-course of oxidation of lipids in human cerebrospinal fluid in vitro [J].
Arlt, S ;
Finckh, B ;
Beisiegel, U ;
Kontush, A .
FREE RADICAL RESEARCH, 2000, 32 (02) :103-114
[2]   Cerebrospinal fluid lipoproteins are more vulnerable to oxidation in Alzheimer's disease and are neurotoxic when oxidized ex vivo [J].
Bassett, CN ;
Neely, MD ;
Sidell, KR ;
Markesbery, WR ;
Swift, LL ;
Montine, TJ .
LIPIDS, 1999, 34 (12) :1273-1280
[3]   VITAMIN-E PROTECTS NERVE-CELLS FROM AMYLOID BETA-PROTEIN TOXICITY [J].
BEHL, C ;
DAVIS, J ;
COLE, GM ;
SCHUBERT, D .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 186 (02) :944-950
[4]  
Borghini I, 1993, Schweiz Arch Neurol Psychiatr (1985), V144, P207
[5]   TOCOPHEROL-MEDIATED PEROXIDATION - THE PROOXIDANT EFFECT OF VITAMIN-E ON THE RADICAL-INITIATED OXIDATION OF HUMAN LOW-DENSITY-LIPOPROTEIN [J].
BOWRY, VW ;
STOCKER, R .
JOURNAL OF THE AMERICAN CHEMICAL SOCIETY, 1993, 115 (14) :6029-6044
[6]   PREVENTION OF TOCOPHEROL-MEDIATED PEROXIDATION IN UBIQUINOL-10-FREE HUMAN LOW-DENSITY-LIPOPROTEIN [J].
BOWRY, VW ;
MOHR, D ;
CLEARY, J ;
STOCKER, R .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (11) :5756-5763
[7]   Metals and neuroscience [J].
Bush, AI .
CURRENT OPINION IN CHEMICAL BIOLOGY, 2000, 4 (02) :184-191
[8]   Graded dietary levels of RRR-gamma-tocopherol induce a marked increase in the concentrations of alpha- and gamma-tocopherol in nervous tissues, heart, liver and muscle of vitamin-E-deficient rats [J].
Clement, M ;
Bourre, JM .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 1997, 1334 (2-3) :173-181
[9]   IRON AND ALUMINUM IN RELATION TO BRAIN FERRITIN IN NORMAL INDIVIDUALS AND ALZHEIMERS-DISEASE AND CHRONIC RENAL-DIALYSIS PATIENTS [J].
DEDMAN, DJ ;
TREFFRY, A ;
CANDY, JM ;
TAYLOR, GAA ;
MORRIS, CM ;
BLOXHAM, CA ;
PERRY, RH ;
EDWARDSON, JA ;
HARRISON, PM .
BIOCHEMICAL JOURNAL, 1992, 287 :509-514
[10]   Oxidized lipoproteins may play a role in neuronal cell death in Alzheimer disease [J].
Draczynska-Lusiak, B ;
Doung, A ;
Sun, AY .
MOLECULAR AND CHEMICAL NEUROPATHOLOGY, 1998, 33 (02) :139-148