Figure 3 Chemical structures of 2,5,7,8-tetramethyl-2-(^-carboxyethyl)-6-hydroxychroman(a-CEHC) and 2,7,8-trimethyl-2-(/3-carboxyethyl)-6-hydroxychroman (7-CEHC).

substantial proportion of the estimated daily intake of 7-tocopherol is excreted in human urine as its 7-CEHC metabolite, but a much smaller proportion of a-tocopherol is excreted as 2,5,7,8-tetramethyl-2-(/3-carboxyethyl)-6-hydroxychroman (a-CEHC) (Figure 3). a-CEHC is excreted in large amounts only when the daily intake of a-tocopherol exceeds 150 mg or plasma concentrations of a-tocopherol are above a threshold of 30-40 mmol l_1. Even then, urinary excretion of a-CEHC is lower than that of 7-CEHC.

It is likely that it is the capacity of a-TTP rather than the plasma a-tocopherol concentration that determines a-tocopherol degradation. Overall, hepatic catabolism of 7-tocopherol appears to be responsible for the relatively low preservation of 7-tocopherol in plasma and tissues, whereas a-TTP-mediated a-tocopherol transfer plays a key role in the preferential enrichment of a-tocopherol in most tissues. Supplementation with a-tocopherol depletes plasma and tissue 7-tocopherol levels. This is likely due to the preferential affinity of a-TTP for a-tocopherol. However, the depletion of 7-tocopherol may also occur because an increase in a-tocopherol may further reduce the incorporation of 7-tocopherol into VLDL, which leaves more 7-tocopherol to be degraded by CYP. On the other hand, 7-tocopherol supplementation may spare a-tocopherol from being degraded.

Plasma (RRR)-a-tocopherol incorporation is a saturable process. Plasma concentrations of a-tocopherol reach a threshold of 30-40 mmoll-1 despite supplementation with high levels (400 mg or greater) of (RRR)-a-tocopherol. Dose-response studies showed that the limitation in plasma a-tocopherol concentration appears to be a result of rapid replacement of circulating with newly absorbed a-tocopherol. Kinetic analysis has shown that the entire plasma pool of a-tocopherol is replaced daily. The highest concentrations of a-tocopherol in the body are in adipose tissues and adrenal glands. Adipose tissues are also a major store of the vitamin, followed by liver and skeletal muscle. The rate of uptake and turnover of a-tocopherol by different tissues varies greatly. Uptake is most rapid into lungs, liver, spleen, kidney, and red cells (in rats, t1=2 < 15 days) and slowest in brain, adipose tissues, and spinal cord (t1/2 < 30 days). Likewise, depletion of a-tocopherol from plasma and liver during times of dietary deficiency is rapid, whereas adipose tissue, brain, spinal cord, and neural tissues are much more difficult to deplete.

The major route for the elimination of tocopherol from the body is via the feces. Fecal tocopherol arises from incomplete absorption, secretion from mucosal cells, and biliary excretion. Excess a-tocopherol as well as forms of vitamin E not preferentially used, such as synthetic racemic isomer mixtures, or 7-tocopherol are eliminated during the process of nascent VLDL secretion in the liver and are probably excreted into bile. In addition to the urinary excretion of 7-tocopherol as 7-CEHC, biliary excretion is an alternative route for elimination of excess 7-tocopherol. This is confirmed by the fact that the ratio of 7- to a-tocopherol in bile is sevenfold higher than in plasma.

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