Dietary vitamin E and tissue labile iron: possible role of superoxide

Vitamin E is capable of attenuating iron-induced oxidative damage although the mechanism is not yet clear. Information available suggests that vitamin E may mediate the generation/levels of superoxide, which may release iron from its protein complex. Free iron has potential to catalyze the formation of reactive hydroxyl radical. In this study, if dietary vitamin E alters mitochondrial superoxide generation and levels of labile iron was studied in rats. One-month-old Sprague-Dawley rats were fed a basal vitamin E-deficient diet supplemented with 0, 20, 200, or 2000 IU vitamin E/kg diet for 90 days. Immediately following sacrifice liver and skeletal muscle were processed to measure the rate of mitochondrial superoxide (hydrogen peoxide) generation, as well as the levels of labile iron and lipid peroxidation products. The results showed that dietary vitamin E dose-dependently reduced the rate of mitochondrial Superoxide generation, as well as the levels of labile iron and lipid peroxidation products. The findings suggest that dietary vitamin E may protect against iron-induced oxidative damage by reducing the generation and/or levels of superoxide, which in turn attenuates iron release from its protein complex.