Cells require lipid soluble substances for their survival and health, but the transport mechanisms that nourishes them is composed mainly of water. As lipids do not dissolve in water, this is potentially problematic. The body overcomes this problem by using proteins to transport the lipids within the aqueous medium of the blood. Vitamin E is a lipid soluble vitamin, and in this regard requires proteins for its transport within the circulation. Vitamin E does not have a specific transport protein, but instead is incorporated into the lipoproteins used to transport cholesterol and fatty acids around the circulation. Much of the vitamin E is transported to the tissues in the low density lipoprotein (LDL) molecule. When the vitamin E containing LDL molecule arrives at the cells it is taken-up through specific carrier mediated mechanisms into the cells interior. Studies comparing the concentration of vitamin E in cells with and without LDL receptors show that the LDL receptor may be an important determinant of correct delivery of vitamin E to cells1.
This is interesting because it has relevance to those individuals with familial hypercholesterolaemia, a condition characterised by a lack of LDL receptors. Such individuals are at high risk of cardiovascular disease because their lipid metabolism is dysfunctional, and as a result they develop atherosclerosis in their arteries. However, evidence from cell culture suggests that such individuals do have the ability to concentrate some vitamin E in their tissues despite a lack of an LDL receptor. This would tend to suggest that some vitamin E may be transferred directly from the LDL particles to the membranes of cells without the need for LDL uptake. The LDL particle is rich in phospholipids containing polyunsaturated fatty acids, and their uptake into cells requires simultaneous delivery of an antioxidant capable of preventing oxidation of these fatty acids. The transport of vitamin iE in the LDL particle provides this protection and thus protects the cells from the potentially toxic effects of oxidised fatty acids and other lipids.
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