COMPARISON OF THE EFFECTS OF DIETARY VITAMIN-E ON IN-VIVO AND IN-VITRO PARAMETERS OF LIPID-PEROXIDATION IN THE RABBIT

被引:23
作者
WISEMAN, SA [1 ]
VANDENBOOM, MAP [1 ]
DEFOUW, NJ [1 ]
WASSINK, MG [1 ]
OPDENKAMP, JAF [1 ]
TIJBURG, LBM [1 ]
机构
[1] UNIV UTRECHT,CTR BIOMEMBRANES & LIPID ENZYMOL,UTRECHT,NETHERLANDS
关键词
VITAMIN-E; PARINARIC ACID; MALONDIALDEHYDE; OXYSTEROLS; LOW DENSITY LIPOPROTEIN; LIPID PEROXIDATION; BIOMARKERS; RABBITS; FREE RADICALS;
D O I
10.1016/0891-5849(95)00078-C
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
This study has investigated the effect of dietary vitamin E on markers of antioxidant status. Four groups of rabbits received diets containing 30 energy percent (en%) total fat (7.8 en% contributed by linoleic acid) for 12 weeks. D,1-alpha tocopheryl acetate was added to the diets to obtain a range of vitamin E concentrations (49, 114, 179, or 775 tocopherol equivalents per kg diet). Increased vitamin E concentrations were demonstrated in plasma lipoproteins and erythrocyte membranes following supplementation, and dietary effects on lipid peroxidation were investigated by (i) monitoring a fluorescent parinaric acid probe incorporated into erythrocyte membranes in vivo, (ii) determination of malondialdehyde and oxysterols in plasma, and (iii) investigation of the susceptibility of low density lipoprotein (LDL) to copper-induced conjugated diene formation in vitro. No effects of vitamin E were observed on parinaric acid oxidation in vivo or on the accumulation of lipid peroxidation products in plasma, but the resistance of LDL to oxidation in vitro increased significantly as vitamin E was supplemented to the diets. Our results demonstrate that under these dietary conditions (7.8 en% linoleic acid) increasing the vitamin E content of plasma and erythrocytes approximately two-fold does not reduce the level of lipid peroxidation in vivo, indicating sufficient antioxidant capacity on the lowest vitamin E diet. In contrast, LDL became more resistant to an extreme oxidative stress applied in vitro. The relevance of these assays to currently proposed mechanisms of atherosclerosis is discussed.
引用
收藏
页码:617 / 626
页数:10
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