RED-CELL VITAMIN-E AND OXIDATIVE DAMAGE - A DUAL ROLE OF REDUCING AGENTS

The purpose of this study was to determine the role of reducing agents in maintaining the integrity of vitamin E-deficient red cells. Three groups of one-month-old male Wistar rats were fed a basal vitamin E-de ficient diet supplemented with either 0, 10 or 100 mg d, 1-alpha-tocop heryl acetate per kg diet for up to 12 weeks. Washed red blood cells ( 5%) were resuspended in saline-phosphate buffer, pH 7.4, and were incu bated at 37 degrees C with or without containing 12.5 mM 2,2'-azobis ( 2amino-propane) dihydrochloride (AAPH), 2.8 mM glucose, 1 mM ascorbic acid, 10 mM hydrogen peroxide (H2O2), 250 mu M dimethylsulfoxide (DMSO ) or 2.8 mM deoxyribose (DR) for up to 20 hours. Addition of either gl ucose, AAPH, ascorbic acid or H2O2 markedly accelerated the rates of h emolysis and lipid peroxidation in the red cells of vitamin E-deficien t rats. On the contrary, both glucose and ascorbic acid were protectiv e against oxidative damage to the red cells of vitamin E-supplemented rats in a dose-dependent manner. Also, vitamin E-supplemented red cell s were more resistant to AAPH and H2O2 than the deficient cells. DMSO or DR had no significant effects on the rates of hemolysis or lipid pe roxidation. Glucose, but not others, maintained or slowed down the los s of glutathione (GSH) during incubation. The results obtained suggest a dual role of ascorbic acid and GSH in the function of vitamin E in maintaining red cell integrity: these reducing agents may exert antiox idant function by participating in vitamin E regeneration when certain levels of vitamin E is maintained, but promote oxidative damage by en hancing free radical generation when vitamin E is low or depleted.