Effects of long-term selenium deficiency on glutathione peroxidase and thioredoxin reductase activities and expressions in rat aorta

被引:67
作者
Wu, QZ [1 ]
Huang, KX [1 ]
Xu, HB [1 ]
机构
[1] Huazhong Univ Sci & Technol, Dept Chem, Wuhan 430074, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
arterial wall; glutathione peroxidase; selenium; thioredoxin reductase;
D O I
10.1016/S0162-0134(03)00058-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
The objective of this work was to determine whether long-term selenium (Se) deficiency might affect the antioxidant capacity of rat aorta, and the activities and expressions of glutathione peroxidase (GPx) and thioredoxin reductase (TR) in rat arterial walls. Weanling male Wister rats were fed Se-deficient or Se-adequate diets for 12 months. For the Se supplementation, sodium selenite was supplemented in drinking water (1 mug Se/ml) for 1 month. The aorta isolated from these groups were used to determine activities and mRNA levels. In comparison with the control, the activity and expression of GPx, superoxide dismutase activity and the total antioxidant capacity were significantly decreased in Se-deficient rats arterial walls. Following Se supplementation, they were restored to different extents'. The content of malondialdehyde was increased markedly in Se-deficient rats. There seems an inverse relationship between the dietary Se and the activity and expression of TR. A positive relationship exists between dietary Se and the antioxidant capacity of rat arterial walls. The activities and expressions of GPx and TR in arterial walls were regulated by selenium by different mechanisms. Regulation of the expression of TR was mediated by reactive oxygen species, but of GPx by selenium status. The thioredoxin system may be the major cellular redox signaling system in rat arteries, rather than the glutathione system. (C) 2003 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:301 / 306
页数:6
相关论文
共 51 条
[2]
ANDERSON TJ, 1995, AM J CARDIOL, V75, P71
[3]
Thioredoxin reductase as a pathophysiological factor and drug target [J].
Becker, K ;
Gromer, S ;
Schirmer, RH ;
Müller, S .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2000, 267 (20) :6118-6125
[4]
Apoptosis of vascular smooth muscle cells in vascular remodelling and atherosclerotic plaque rupture [J].
Bennett, MR .
CARDIOVASCULAR RESEARCH, 1999, 41 (02) :361-368
[5]
Effect of selenium on rat thioredoxin reductase activity - Increase by supranutritional selenium and decrease by selenium deficiency [J].
Berggren, MM ;
Mangin, JF ;
Gasdaska, JR ;
Powis, G .
BIOCHEMICAL PHARMACOLOGY, 1999, 57 (02) :187-193
[6]
ATHEROSCLEROSIS - BASIC MECHANISMS - OXIDATION, INFLAMMATION, AND GENETICS [J].
BERLINER, JA ;
NAVAB, M ;
FOGELMAN, AM ;
FRANK, JS ;
DEMER, LL ;
EDWARDS, PA ;
WATSON, AD ;
LUSIS, AJ .
CIRCULATION, 1995, 91 (09) :2488-2496
[7]
TISSUE-SPECIFIC REGULATION OF SELENOENZYME GENE-EXPRESSION DURING SELENIUM DEFICIENCY IN RATS [J].
BERMANO, G ;
NICOL, F ;
DYER, JA ;
SUNDE, RA ;
BECKETT, GJ ;
ARTHUR, JR ;
HESKETH, JE .
BIOCHEMICAL JOURNAL, 1995, 311 :425-430
[8]
REGULATION OF SELENOPROTEINS [J].
BURK, RF ;
HILL, KE .
ANNUAL REVIEW OF NUTRITION, 1993, 13 :65-81
[9]
Altered eicosanoid biosynthesis in selenium-deficient endothelial cells [J].
Cao, YZ ;
Reddy, CC ;
Sordillo, LM .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 28 (03) :381-389
[10]
TISSUE-SPECIFICITY OF SELENOPROTEIN GENE-EXPRESSION IN RATS [J].
CHRISTENSEN, MJ ;
CAMMACK, PM ;
WRAY, CD .
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, 1995, 6 (07) :367-372