THE ROLE OF FREE-RADICALS AS MEDIATORS OF ENDOTHELIAL-CELL INJURY IN HYPERHOMOCYSTEINEMIA

被引：22

作者：

CLARKE, R ^{[1
]}

NAUGHTEN, E ^{[1
]}

CAHALANE, S ^{[1
]}

SULLIVAN, KO ^{[1
]}

MATHIAS, P ^{[1
]}

MCCALL, T ^{[1
]}

GRAHAM, I ^{[1
]}

机构：

[1] ADELAIDE HOSP,DEPT CARDIOL,PETER ST,DUBLIN 8,IRELAND

来源：

IRISH JOURNAL OF MEDICAL SCIENCE | 1992年 / 161卷 / 09期

关键词：

D O I：

10.1007/BF02940559

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hyperhomocysteinemia has been suggested as a potent new risk factor for premature cardiovascular disease. Homocsyteine can induce endothelial cell injury but the mechanism is not understood. The purpose of this study was to evaluate the role of free radicals as potential causes of endothelial cell injury in a case-control study of obligate heterozygotes for cystathionine beta-synthase deficiency. Firstly, free radical production as measured by neutrophil chemiluminescence in obligate heterozygotes for cystathionine beta-synthase deficiency was compared with age- and sex-matched normal subjects. Secondly, the response or the cellular antioxidant system was examined by measuring the enzymes superoxide dismutase and glutathione peroxidase, their cofactors (selenium, copper), vitamin E and vitamin A in heterozygotes and normal subjects. Analyses of neutrophil chemiluminescence, vitamin A and E, glutathione peroxidase, selenium and copper showed no difference between heterozygotes and controls. While superoxide dismutase activity was higher in heterozygotes than normal subjects, the difference did not reach statistical significance and the hypothesis of excess free radical production as a mechanism of injury was not confirmed. However, further examination of superoxide dismutase activity in a larger number of subjects would be of interest.

引用

页码：561 / 564

页数：4

共 31 条

[1] Mudd S.H., Levy H.L., Skovby F., Disorders of Transulfura- tion, The Metabolic Basis of Inherited Disease, pp. 693-734, (1989)
[2] Boers G.H., Smals A.G., Trijbels F.J., Et al., Heterozygosity for homocystinuria in premature peripheral and cerebral occlusive arterial disease, N. Engl. J. Med., 313, pp. 709-15, (1985)
[3] Brattstrom L.E., Hardebo I.E., Hultberg B.L., Moderate homocysteinemia - a possible risk factor for arteriosclerotic cere- brovascular disease, Stroke, 15, pp. 1012-6, (1984)
[4] Clarke R., Daly L., Robinson K., Naughten E., Cahalane S., Fowler B., Graham I., Hyperhomosysteinemia: an independent risk factor for vascular disease, N. Engl. J. Med., 324, pp. 1149-55, (1991)
[5] Malinow M.R., Kang S.S., Taylor L.M., Et al., Prevalence of hyperhomocyst(e)inemia in patients with peripheral arterial occlusive disease. Circulation, 79, pp. 1180-8, (1989)
[6] Harker L.A., Slichter S.J., Scott C.R., Ross R., Homocysteinemia, vascular injury and arterial thrombosis, N. Engl. J. Med., 291, pp. 537-43, (1974)
[7] McCully K.S., Homocysteine theory of arteriosclerosis
[8] development and current status, Arteriosclerosis Rev., 11, pp. 157-246, (1983)
[9] Wall R.T., Harlan J.M., Harker L.A., Striker G.E., Homocys- teine-induced endothelial cell injury in vitro: a model for the study of vascular injury, Thromb. Res., 18, pp. 113-21, (1989)
[10] Starkebaum G., Harlan J.M., Endothelial cell injury due to copper- catalyzed hydrogen peroxide generation from homocysteine, J. Clin. Invest., 77, pp. 1370-76, (1986)

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