Metabolic Functions Of Vitamin E

The best-established function of vitamin E is as a lipid-soluble antioxidant in plasma lipoproteins and cell membranes. Many of the antioxidant actions are unspecific, and a number of synthetic antioxidants have a vitamin E-sparing effect. There is considerable overlap between the antioxidant roles of vitamin E and selenium (Section 4.3.2).

A number of studies have shown that a-tocopherol has a role in modulation of gene expression and regulation of cell proliferation (Section 4.3.3), suggesting that the potential beneficial effects of vitamin E against heart disease and cancer (Section 4.6.2) may not be because of its antioxidant action.

There is some evidence that tocopherols have a specific function in cell membranes; the phytyl side chain of RRR-a-tocopherol can interact closely with the methylene-interrupted ds-double bonds of arachidonic acid and other long-chain polyunsaturated fatty acids in membranes, both stabilizing membrane structure and also protecting the fatty acids from oxidative damage. The membrane phospholipids of fibroblasts grown in culture contain more arachidonate, and less linoleate, when grown in the presence of adequate amounts of a-tocopherol. This seems to be a specific effect on phospholipid synthesis and is not reflected in the fatty acid content of neutral lipids (Giasuddin and Diplock, 1981). a-Tocopherol forms a 1:1 complex with lysophospholipids and free fatty acids formed by the action of membrane phospholipases, thus negating the detergent-like action that might otherwise disrupt the membrane (Wang and Quinn, 1999, 2000).

It was noted in Section 4.1 that the tocotrienols can be considered to be derivatives of mevalonate, the product of HMG CoA reductase, which is the key regulatory enzyme of cholesterol synthesis. Dietary tocotrienols have a cholesterol-lowering effect; they act by reducing the activity of HMG CoA re-ductase. The main effect is posttranslational; tocotrienols cause an increased rate of catabolism of the enzyme protein (Parker et al., 1993; Theriault et al., 1999). Tocotrienols also induce cell cycle arrest in tumor cell lines in culture and induce apoptosis (Yu et al., 1999).

As well as being an end-product of the oxidation of a-tocopherol, a-tocopherol quinone (see Figure 4.3) is the cofactor for the mitochondrial fatty acid desaturation/elongation pathway, and it has been suggested that the severe neurological degeneration in patients with a genetic lack of a-tocopherol transfer protein or abetalipoproteinemia (Section 4.4.2) is caused by failure of synthesis oflong-chain polyunsaturated fatty acids (Infante, 1999).

The main metabolite of y-tocopherol is 2,7,8-trimethyl-2-(^-carboxyeth-yl)-6-hydroxychroman (y -CEHC), which is excreted in the urine. It has potentially physiologically significant natriuretic activity, whereas the corresponding metabolite of a-tocopherol, which is formed in increasing amounts as intake increases, is inactive (Jiang et al., 2001).

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