Oxidative damage in the red cells of vitamin E-deficient rats.

One month-old male Sprague-Dawley rats were maintained on a basal vitamin E-deficient diet supplemented with either 0 or 50 ppm vitamin E for 5 months. Washed red blood cells were resuspended in phosphate buffered-saline, pH 7.4, that contained 0-50 mM glucose and 0-20 mM ethylenediamine tetraacetic acid (EDTA), and were incubated at 37 degrees C for up to 22 h. Contrary to expectations, glucose in the incubation medium accelerated, rather than retarded, the rates of hemolysis, lipid peroxidation and methemoglobin formation in the vitamin E-deficient cells. EDTA, on the other hand, partially inhibited the extent of oxidative damage. Vitamin E-supplemented cells were resistant to oxidative damage in the presence or absence of glucose and/or EDTA. The levels of reduced glutathione (GSH) and activity of catalase were decreased faster in the vitamin E-deficient cells than the supplemented cells, and the rates of their decline were slowed down by either glucose or EDTA. The activities of GSH peroxidase and superoxide dismutase were not significantly altered in the red cells of either group during incubation. The results obtained suggest that reactive oxygen species and reduced metal ions play important roles in initiating oxidative damage to the red cells of vitamin E-deficient rats. However, the agent responsible for initiating the hemolytic event has yet to be established.