In three people with ataxia and vitamin E deficiency (AVED) secondary to a defect in the α-TTP gene (Cavalier et al., 1998), the half-lives for both RRR- and SRR-α-tocopherols were approximately 13 hours (Traber et al., 1994b). These studies demonstrate that RRR- and SRR-α-tocopherols in the AVED patients disappear at the same rate as SRR-α-tocopherol in the control subjects. This suggests that α-TTP, which is defective in the AVED patients, is responsible for the longer half-life of RRR-α-tocopherol in the control subjects. It was estimated that resecretion of RRR-α-tocopherol by the liver in the control subjects resulted in the daily replacement of nearly all of the circulating RRR-α-tocopherol. Thus, the liver maintains plasma RRR-α-tocopherol concentrations by a continuous resecretion process. In contrast, other forms of vitamin E (e.g., SRR-α- and γ-tocopherols) are not resecreted into the plasma.
Oxidation Products. α-Tocopherol can be oxidized to the tocopheroxyl radical—one-electron oxidation product—which can be reduced back to the unoxidized form by reducing agents such as vitamin C. Further oxidation of the tocopheroxyl radical forms