Tissues are dependent upon uptake of vitamin E from plasma (Traber, 1999). No specific plasma transport proteins have been described; therefore, it is likely that the mechanisms of lipoprotein metabolism determine the delivery of vitamin E to tissues. Tissues probably acquire vitamin E by several major routes: (1) during lipoprotein lipase mediated triglyceride-rich lipoprotein catabolism; (2) during low-density lipoprotein (LDL) uptake via the LDL receptor; (3) via high-density lipoprotein (HDL)-mediated delivery systems; and (4) by nonspecific transfers between lipoproteins and tissues. Vitamin E rapidly transfers between various lipoproteins and also between lipoproteins and membranes, which may enrich membranes with vitamin E. The human plasma phospholipid transfer protein accelerates this process (Kostner et al., 1995).
Human tissue vitamin E contents have been reported mostly from relatively easy-to-sample tissues (e.g., adipose tissue and buccal mucosal cells) (Handelman et al., 1994; Kayden et al., 1983; Parker, 1988; Peng et al., 1994; Traber and Kayden, 1987; Traber et al., 1987). To obtain a variety of human tissues, Burton et al. (1998) enlisted two terminally ill subjects who agreed to daily supplementation with deuterated (d3-RRR- and d6-all rac) α-tocopherols. At death, an autopsy was performed to obtain various tissues. One subject took 15 mg (32 µmol) d3-RRR- and 15 mg (32 µmol) d6-all rac-α-tocopheryl acetate for 361 days, while the other took 150 mg (320 µmol) d3-RRR- plus 150 mg (320 µmol) d6-all rac-α-tocopheryl acetates for 615 days. Tissue unlabeled α-tocopherol concentrations were generally similar in both patients. In the patient who consumed 30 mg (64 µmol)/day labeled vitamin E for 1 year, about 5.9 ± 2.2 (SD) percent of the tissue vitamin E was labeled, while about 65 ± 10 (SD) percent was labeled in the patient who consumed a total of 300 mg (640 µmol) daily for 2 years. The RRR/all rac ratios in plasma and tissues at autopsy were similar in both patients (2.06 and 1.71 ± 0.24 (SD), respectively, on the lower dose and 2.11 and 2.01 ± 0.17 (SD), respectively, on the higher dose).
The results indicate that the RRR-stereoisomer has roughly twice the availability of the all rac forms. The effect of 300 mg vitamin E supplementation was to increase plasma α-tocopherol concentrations threefold and to at least double most tissue concentrations, while supplementation with 30 mg had little effect on either plasma or tissue α-tocopherol concentrations. These data suggest that tissue α-tocopherol concentrations largely reflect changes in plasma concentrations of α-tocopherol and that larger doses increase tissue