Metabolism Of Vitamin E

The absorption of vitamin E is relatively poor - only some 20% to 40% of a test dose is normally absorbed from the small intestine, in mixed lipid micelles with other dietary lipids. This absorption is enhanced by medium-chain triglycerides and inhibited by polyunsaturated fatty acids, possibly because of chemical interactions between tocopherols and polyunsaturated fatty acids or their peroxidation products in the intestinal lumen. Esters are hydrolyzed in the intestinal lumen by pancreatic esterase and also by intracellular esterases in the mucosal cells.

In intestinal mucosal cells, all vitamers of vitamin E are incorporated into chylomicrons, and tissues take up some vitamin E from chylomicrons. Most, however, goes to the liver in chylomicron remnants. a -Tocopherol, whichbinds to the liver a -tocopherol transfer protein, is then exported in very low-density lipoprotein (VLDL) and is available for tissue uptake (Traber and Arai, 1999; Stocker andAzzi, 2000). Later, it appears in low-density lipoprotein (LDL) and high-density lipoprotein, as a result of metabolism of VLDL in the circulation. The other vitamers, which do not bind well to the a-tocopherol transferprotein, are not incorporated into VLDL, but are metabolized in the liver and excreted. This explains the lower biological potency of the other vitamers, despite similar, or higher, in vitro antioxidant activity.

The affinities of a-tocopherol transfer protein for the other vitamers (relative to RRR-a-tocopherol = 1, and based on competition with RRR-a-toco-pherol) are f -tocopherol, 0.38; y-tocopherol, 0.09; 5-tocopherol, 0.02; SRR-a-tocopherol, 0.11; and a-tocotrienol, 0.09. As a result, whereas the half-life of a-tocopherol in the circulation is 48 hours, that of f - and y-tocopherol (and the other vitamers) is only of the order of 13 to 15 hours. In patients with ataxia and vitamin E deficiency caused by a genetic lack of a-tocopherol transfer

CH3 or ubiquinone CH3

tocopherol tocopheroxyl radical

CH3 or ubiquinone CH3

tocopherol tocopheroxyl radical

CH3 CH3

tocopherol quinone tocopherol hydroqulnone

Figure 4.3. Reaction of tocopherol with lipid peroxides; the tocopheroxyl radical can be reduced to tocopherol or undergo irreversible onward oxidation to tocopherol quinone.

CH3 CH3

tocopherol quinone tocopherol hydroqulnone

Figure 4.3. Reaction of tocopherol with lipid peroxides; the tocopheroxyl radical can be reduced to tocopherol or undergo irreversible onward oxidation to tocopherol quinone.

protein (Section 4.4.2), the half-life of plasma a-tocopherol is of the order of 13 hours (Hosomi et al., 1997).

Because vitamin E is transported in lipoproteins secreted by the liver, the plasma concentration depends to a great extent on total plasma lipids. Erythrocytes may also be important in transport, because there is a relatively large amount of the vitamin in erythrocyte membranes, and this is in rapid equilibrium with plasma vitamin E. There are two mechanisms for tissue uptake of the vitamin. Lipoprotein lipase releases the vitamin by hydrolyzing the tri-acylglycerol in chylomicrons and VLDL, whereas separately there is receptor-mediated uptake of LDL-bound vitamin E. Studies in knockout mice suggest that the main mechanism for tissue uptake of vitamin E from plasma lipoproteins is byway of the class B scavenger receptor (Mardones et al., 2002).

Retention within tissues depends on intracellular binding proteins which, like the liver a-tocopherol transfer protein, have the highest affinity for RRR-a-tocopherol. The retention of a-tocopherol in tissues varies. In the lungs the vitamin has a half-life of 7.6 days, in liver 9.8 days, in skin 23.4 days, in brain 29.4 days, and in the spinal cord 76.3 days (Ingold et al., 1987).

As shown in Figure 4.3, tocopherol can undergo reversible oxidation to an epoxide, followed by ring cleavage to yield a quinone, which is reduced to the hydroquinone and conjugated with glucuronic acid, for excretion in the bile, which is the major route of excretion. The side chain of the quinone and hydroquinone may be oxidized by p-oxidation, and small amounts of these oxidation products (carboxyethyl-hydroxychromans) and their conjugates are excreted in the urine. This is generally a minor route of metabolism, accounting for only about 1% of a test dose of labeled a-tocopherol, although larger amounts of the oxidation products of the other vitamers are excreted in urine. There may also be significant excretion of the vitamin by the skin. After the administration of chylomicron-incorporated [3H] a-tocopherol to rats, there is not only a significant accumulation and retention of radioactivity in the skin, but also on the outer surface and in the fur (Shiratori, 1974).

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