ERYTHROCYTES FROM MAGNESIUM-DEFICIENT HAMSTERS DISPLAY AN ENHANCED SUSCEPTIBILITY TO OXIDATIVE STRESS

被引:73
作者
FREEDMAN, AM
MAK, IT
STAFFORD, RE
DICKENS, BF
CASSIDY, MM
MUESING, RA
WEGLICKI, WB
机构
[1] GEORGE WASHINGTON UNIV, MED CTR,LIPID RES CTR,DIV EXPTL MED,ROSS HALL, ROOM 402,2300 EYE ST NW, WASHINGTON, DC 20037 USA
[2] GEORGE WASHINGTON UNIV, MED CTR, DEPT MED, WASHINGTON, DC 20037 USA
[3] GEORGE WASHINGTON UNIV, MED CTR, DEPT PHYSIOL, WASHINGTON, DC 20037 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1992年 / 262卷 / 06期
关键词
MAGNESIUM DEFICIENCY; FREE RADICALS; LIPID ALTERATIONS; VITAMIN-E;
D O I
10.1152/ajpcell.1992.262.6.C1371
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Previous studies in our laboratory have indicated a role for free radical participation in magnesium deficiency cardiomyopathy. We have demonstrated the ability of various antioxidant drugs and nutrients to protect against magnesium deficiency-induced myocardial injury. In this study, we have examined erythrocytes from normal and magnesium-deficient animals and compared their susceptibility to an in vitro oxidative stress. Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group also received vitamin E in doses of 10 and 25 mg as subcutaneous implants. Erythrocytes obtained after 14 days on the diet were exposed to an exogenous hydroxyl (.OH) radical generating system (dihydroxyfumarate not-equal Fe3+ ADP) at 37-degrees-C for 20 min. Erythrocyte crenation was observed and quantified by scanning electron microscopy. Lipid peroxidation, hemolysis (%), and intracellular glutathione levels were determined. In addition, serum lipid changes and membrane phospholipids were characterized. Our data demonstrate that erythrocytes from magnesium-deficient animals are more susceptible to free radical injury, supporting our hypothesis that magnesium deficiency reduces the threshold antioxidant capacity.
引用
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页码:C1371 / C1375
页数:5
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