tocopheryl quinone, the two-election oxidation product. The tocopheryl quinone is not converted in any physiologically significant amounts back to tocopherol (Moore and Ingold, 1997). Other oxidation products, including dimers and trimers as well as adducts (Kamal-Eldin and Appelqvist, 1996), are formed during in vitro oxidation; their importance in vivo is unknown.
Other Metabolites. Vitamin E metabolites in human urine include both 2,5,7,8-tetramethyl-2-(2 ′-carboxyethyl)-6-hydroxychroman (α-CEHC) derived from α-tocopherol (Schultz et al., 1995, 1997) and 2,7,8-trimethyl-2- (2 ′-carboxyethyl)-6-hydroxychroman (γ-CEHC) derived from γ-tocopherol (Murray et al., 1997; Wechter et al., 1996). These metabolites result from degradation of the phytyl tail; the chromanol ring is unchanged and thus they are not oxidation products of vitamin E. It is unknown where these metabolites are formed.
Urinary Excretion. Increasing doses of supplemental vitamin E in humans result in increasing urinary excretion of the α-CEHC metabolite (Schultz et al., 1995). Interestingly, three times as much all rac-α-tocopherol as compared with RRR-α-tocopherol is excreted as α-CEHC, while twice as much RRR-α-tocopherol is found in the plasma (Traber et al., 1998), suggesting that these urinary metabolites may be indicators of nonpreferentially utilized vitamin E forms. Indeed, Swanson et al. (1998, 1999) showed that about half of the ingested γ-tocopherol is metabolized and excreted as γ-CEHC. This metabolite has been reported to inhibit the potassium channel and increase urinary sodium excretion (Kantoci et al., 1997; Murray et al., 1997; Wechter et al., 1996). Thus, urinary excretion of CEHC may indicate excess vitamin E intake. However, this has yet to be definitively demonstrated, and no physiological role for the in vivo effects of γ-CEHC have been established.
Fecal Excretion. The major route of excretion of ingested vitamin E is fecal elimination because of its relatively low intestinal absorption. Excess α-tocopherol, as well as forms of vitamin E not preferentially used, are probably excreted unchanged in bile (Traber and Kayden, 1989). Leo et al. (1995) report α-tocopherol concentrations in human bile of 8.4 ± 0.9 (SD) µmol/L (361 ± 38.7 µg/dL) compared with 23.2 ± 1.7 (SD) µmol/L (998 ± 73 µg/dL) in plasma.