Vitamin C (L-ascorbic acid) protects human health by scavenging toxic free radicals and other reactive oxygen species formed in cell metabolism. The surplus supplementation of vitamin C, however, may be harmful to health because the level of 8-oxoguanine and 8-oxoadenine in lymphocyte DNA varies remarkably. In the process of the kinetic investigation on the 2,20-azobis(2-amidinopropane dihydrochloride) (AAPH)-induced autoxidation of glycerol trioleate (GtH) in the micelles of cetyl trimethyl ammonium bromide (CTAB), sodium dodecyl sulfate (SDS) and Triton X-100, the addition of vitamin C accelerates the autoxidation of GtH even in the absence of the free radical initiator, AAPH. The initiating rate, Ri, of vitamin C (VC)-induced autoxidation of GtH is related to the micelle charge, i.e. Ri=14.4×10-6 [VC] s-1 in SDS (anionic micelle), Ri＝1961×10-6 [VC] s-1 in Triton X-100 (neutral micelle) and Ri is a maximum in CTAB (cationic micelle) when the vitamin C concentration is ～300μM. Thus, vitamin C can initiate autoxidation of GtH in micelles, especially in the neutral one. Moreover, the attempt to explore whether -tocopherol (TocH) could rectify vitamin C-induced autoxidation of GtH leads us to find that the rate constant of TocH reacting with the anionic radical of vitamin C (VC.), k inh, is 103 M-1 s-1, which is less than that of the-tocopherol radical (Toc.) with vitamin C (kinh=105 M-1 s1). Thus, the equilibrium constant of the reaction Toc.þVC ÐTocH=VC. is prone strongly to the regeneration of Toc. by vitamin C rather than the reverse reaction