We studied the location of α-tocopherol(α-Toc) in liposome membranes, and dynamics of radical trapping and tocopherol recycling by ascorbic acid (AsA). No specific interaction was suggested to occur between the OH-group of α-Toc and the polar interfacial region of the bilayer, because of the absence of stretching bands of P = O and C = O of phosphatidylcholine by incorporation of α-Toc into liposomes, and no difference of the spin-lattice relaxation times at the 5a-position of α-Toc between positively and negatively charged liposomes. Low exposure of the chromanol at the surface of liposome membranes was supposed by little interaction with acrylamide, a water-soluble fluorescene quencher with a very low capacity to penetrate through phospholipid bilayers. Since the oxidation rate of α-Toc by positively charged Fe^<3+> was 150 times slower in negatively charged liposomes than in negatively charged SDS micelles, less than 0.65 mol% of the OH-groups of α-Toc was probably exposed at the membrane surface of liposomes. The lack of difference in the oxidation rates of α-Toc in liposomes in gel state and liquid crystalline state suggested that the OH-group was not located deeply in the hydrophobic region of membranes. Among the n-(N-oxy-4,4'-dimethyloxazolidine-2-yl) stearic acids (n-NS) labeled at different depths of membranes, 5-NS most effectively quenched the intrinsic fluorescence of α-Toc, indicating that the OH-group of α-Toc is located in a position corresponding to an inner 5-methylene carbon under the surface, where the OH-group may most efficiently trap the lipid peroxy-radicals floating up from the inner membrane core. The lipid peroxy-radicals were confirmed to float up to the membrane surface, because AsA was rapidly oxidized by 2,2'-azobis-(dimethylvaleronitrile)(AMVN), a hydrophobic radical precursor, when negatively charged AsA was ionically trapped at the positively charged surface of the liposome membranes. AsA completely suppressed the consumption of α-Toc by AMVN-induced lipid peroxidation in negatively charged liposomes. However, AsA did not penetrate into negatively charged membranes, because the ESR spectra of 5-NS and 16-NS labeled in these liposomes were not affected by the addition of AsA. These findings indicate that α-Toc is oxidized just under the membrane surface by lipid radicals, and then floats up to the surface, where it is regenerated to α-Toc by AsA.