ANTIOXIDANTS, VON-WILLEBRAND-FACTOR AND ENDOTHELIAL-CELL INJURY IN HYPERCHOLESTEROLEMIA AND VASCULAR-DISEASE

被引:35
作者
BLANN, AD
MAXWELL, SRJ
BURROWS, G
MILLER, JP
机构
[1] QUEEN ELIZABETH HOSP, DEPT MED, BIRMINGHAM B15 2TH, W MIDLANDS, ENGLAND
[2] UNIV S MANCHESTER HOSP, DEPT CHEM PATHOL, MANCHESTER M20 8LR, LANCS, ENGLAND
[3] UNIV S MANCHESTER HOSP, DEPT MED, MANCHESTER M20 8LR, LANCS, ENGLAND
关键词
VON WILLEBRAND FACTOR; ANTIOXIDANTS; HYPERCHOLESTEROLEMIA; ATHEROSCLEROSIS; GLUTATHIONE PEROXIDASE;
D O I
10.1016/0021-9150(95)05541-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The relationship between antioxidants and endothelial cell injury was examined in 119 patients with (n = 48) or without (n = 71) vascular disease who were attending a hyperlipidaemia clinic. Serum levels of total antioxidant capacity, glutathione peroxidase (a protein antioxidant), von Willebrand factor (vWf, a specific endothelial cell product and marker of injury) and routine lipids were measured in the patients and from 58 healthy controls. Compared to controls, total antioxidant capacity (P < 0.01) and glutathione peroxidase (P < 0.0001) were lower whilst vWf was higher (P < 0.0001) amongst the patients. Comparing patients with and without vascular disease, glutathione peroxidase was lower (P < 0.03) and vWf was higher (P < 0.05) in the presence of vascular disease but there was no difference in levels of serum lipids or total antioxidant capacity. vWf and glutathione peroxidase were inversely correlated (r = -0.26, P < 0.005). We conclude that patients with hypercholesterolaemia have reduced antioxidant capacity and this is most severe in patients with clinically apparent vascular disease. This, linked to the finding of increased vWf in hypercholesterolaemia with highest levels in those patients with vascular disease, suggests that loss of antioxidant capacity may expose the vascular endothelium to excess oxidative damage. These results suggest a link between hypercholesterolaemia, impaired ability to resist free radical attack, and the development of atherosclerosis.
引用
收藏
页码:191 / 198
页数:8
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