Evidence that dimethyl sulfoxide inhibits defects of copper deficiency by inhibition of glycation

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 examine this conclusion further, rats were fed Cu-adequate (6.4 μg/g) and -deficient (0.5 μg/g) diets and given water with or without 5% 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 (Hb A 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 Hb A 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.