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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #60470


item Saari, Jack

Submitted to: Nutrition Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/1/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: Prior research has indicated that defects seen in dietary copper deficiency, such as heart enlargement and anemia, may be caused by damage from free radicals, highly reactive chemicals that are by-products of the body's use of oxygen. One supporting piece of evidence has been that defects of copper deficiency can be ameliorated by the feeding of substances, such as dimethyl sulfoxide (DMSO), that destroy free radicals. To further examine this finding, we fed DMSO to rats consuming a copper- deficient diet and looked for evidence of free radical damage to lipids. Two indices of free radical damage to lipids revealed that, although copper deficiency enhances such damage, DMSO does not reduce it. However, use of an index of damage caused by the undesirable binding of sugar to protein, termed glycation, indicated that DMSO did ameliorate that type of damage. We conclude that, although free radical damage occurs in copper deficiency, DMSO feeding is not beneficial to copper deficient animals by preventing free radical damage, but rather by amelioration of glycation.

Technical Abstract: Prior studies have indicated that dimethyl sulfoxide (DMSO), when fed to rats, can inhibit the cardiac enlargement and anemia of a concurrent dietary copper (Cu) deficiency. Because DMSO is capable of chemically destroying the hydroxyl radical, its inhibition of defects of Cu deficiency was taken as evidence that those defects resulted from oxidative stress. To further examine this conclusion, rats were fed Cu- adequate (6.4 ug/g) and -deficient (0.5 ug/g) diets and given water with or without 5 percent DMSO. Two additional groups of rats were pair-fed to test for the effects of reduced food intake caused by DMSO. To test for mechanism of action of DMSO, indices of lipid peroxidation and nonenzymatic glycosylation of protein (glycation) were measured. Compared to Cu-adequate rats, Cu-deficient rats were anemic and had enlarged hearts, increased serum malondialdehyde (MDA), increased heart thiobarbituric acid reactive substances (TBARS) and an enhanced percentage of glycated hemoglobin (HbA**1). Both DMSO administration and pair feeding ameliorated the anemia of Cu deficiency; pair feeding reduced the cardiac enlargement of Cu deficiency. Neither DMSO nor pair feeding inhibited the rise in serum MDA or heart TBARS, but both caused a similar degree of inhibition of the rise in HbA**1. Although dietary Cu deficiency is associated with an increase in products of peroxidation, the inhibition of defects by DMSO appears to be related to food restriction and inhibition of glycation.