AJP - Cell Physiology, Vol 262, Issue 6 C1371-C1375, Copyright © 1992 by American Physiological Society
Erythrocytes from magnesium-deficient hamsters display an enhanced susceptibility to oxidative stress
A. M. Freedman, I. T. Mak, R. E. Stafford, B. F. Dickens, M. M. Cassidy, R. A. Muesing and W. B. Weglicki
Department of Medicine, George Washington University Medical Center, Washington, DC 20037.
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 to 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.
