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Disorders that develop in animals with vitamin E deficiency are assumed to be related to biomembrane damage (1). We can find such impaired erythrocyte (red blood cell, RBC) membranes deficient in vitamin E (2), because vitamin E-deficient RBCs show an increased susceptibility when exposed to oxidant stress, such as dialuric acid (2-4) and hydrogen peroxide (5-7). Vitamin E, a constituent of biologi cal membranes, probably plays a physiological role as a biological anti-oxidant in protecting biomembranes containing large amounts of polyunsaturated fatty acids from peroxidative damage (8). However, the mechanism for peroxidative damages in vitamin E-deficient RBCs has never been precisely explained, because there are few measurements for determinating lipid peroxidation resulting in membrane damage. In 1962, Vassil'ev and Vichutinskii (9) reported that ultra-weak chemilu minescence is generated during lipid peroxidation. Recently, the quantitative determination of light emission during lipid peroxidation has revived interest in chemiluminescence from living tissues (10-12). This paper deals with chemilumines cence in vitamin E-deficient RBCs with radical attacks by a xanthine oxidase reaction that generates superoxide free radicals. Wistar strain male rats were fed on a vitamin E-deficient diet for 12 or more weeks. The vitamin E-deficient diet consisted of 36% corn starch, 25% vitamin-free casein, 10% alpha starch of wheat, 8% powdered filter paper, 6% salt mixture, 5% granulated sugar, 2% vitamin mixture and 8 % stripped corn oil (from Tama Seikagaku, Co., Ltd.); the salt mixture provided: K, 692mg; P, 579mg; Ca, 411mg;

journal of nutritional science and vitaminology

Chemiluminescence in vitamin E-deficient erythrocytes initiated by xanthine oxidase reaction, in relation to the accumulation of thiobarbituric acid reactive substances.