Dietary vitamin E and C supplementation prevents fructose induced hypertension in rats

被引:0
作者
S. Vasdev
V. Gill
S. Parai
L. Longerich
V. Gadag
机构
[1] Memorial University of Newfoundland,Department of Medicine, Health Sciences Centre
[2] Memorial University of Newfoundland,Discipline of Laboratory Medicine, Health Sciences Centre
[3] Memorial University of Newfoundland,Division of Community Health, Health Sciences Centre
来源
Molecular and Cellular Biochemistry | 2002年 / 241卷
关键词
aldehydes; vitamin E; vitamin C; hypertension;
D O I
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中图分类号
学科分类号
摘要
In fructose-induced hypertension in Wistar-Kyoto (WKY) rats, excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing cytosolic free calcium and blood pressure. The thiol compound N-acetyl cysteine prevents fructose-induced hypertension by binding excess endogenous aldehydes and normalizing membrane Ca2+ channels and cytosolic free calcium. The aim of the present study was to investigate whether dietary supplementation of vitamin E and vitamin C which are known to increase tissue glutathione, a storage form of cysteine, prevents this hypertension and its associated biochemical and histopathological changes. Starting at 7 weeks of age, animals were divided into four groups of six animals each and treated as follows: control group, normal diet and normal drinking water; fructose group, normal diet and 4% fructose in drinking water; fructose + vitamin E group, diet supplemented with vitamin E (34 mg/kg feed) and 4% fructose in drinking water; fructose + vitamin C group, diet supplemented with vitamin C (1000 mg/kg feed) and 4% fructose in drinking water. At 14 weeks, systolic blood pressure, platelet [Ca2+]i and kidney and aortic aldehyde conjugates were significantly higher in the fructose group. These animals also displayed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. Dietary vitamin E and C supplementation in fructose-treated WKY rats prevented the increase in systolic blood pressure by normalizing cytosolic [Ca2+]i and kidney and aortic aldehyde conjugates and preventing adverse renal vascular changes.
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页码:107 / 114
页数:7
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