Vitamin E consists of 8 isomers that share the same biological activity as α-tocopherol. The isomers are α-, β-, γ- and δ-tocopherol and α-, β-, γ- and δ-tocotrienol. The isomers possess slightly different biological activities in humans. For example, γ-tocopherol has 50 % of the antioxidant activity of α-tocopherol and 10 % of the biological activity, the latter as assessed by the ability to prevent vitamin E deficiency symptoms in animal models. Vitamin E acts as an antioxidant by reacting with peroxyl radicals formed during lipid peroxidation, and the subsequent radical is resonance stabilised thus preventing a free radical chain reaction. The usefulness of α-tocopherol stems from the fact that it reacts with peroxyl radicals more readily that polyunsaturated fatty acids and so limits membrane oxidative damage. Ascorbic acid, glutathione or uric acid can regenerate vitamin E, or two α-tocopheroxy radicals can react together to form a dimmer.
The biological activity of vitamin E as well as its antioxidant function relies on the absorption and subsequent transport of vitamin E to the tissues. Because vitamin E is hydrophobic in nature, special mechanisms exist in order to allow this to occur in the water soluble environments of the gut and plasma. Absorption of vitamin E is estimated to be around 70 % of the intake dose, a process that is dependent on the formation of micelles by bile acid secretion. In this way vitamin E is solubilised much like any other dietary lipid. That vitamin E cannot be absorbed without this process has been demonstrated in children with cholestatic disease. Once in micelles, vitamin E passes into enterocytes in a passive process with dietary lipids. Vitamin E is then secreted into chylomicrons and is absorbed to the lymphatic system where it subsequently passes to the blood.
Some vitamin E is transferred to tissues directly from the chylomicrons as normal chylomicron catabolism occurs via lipoprotein lipase. During this process, depletion of chylomicrons of their lipids to muscle and adipose tissue results in chylomicron remnants. Adipose tissue and muscle receive most of their lipids content during this chylomicron catabolisation, and vitamin E not absorbed to muscle or adipose tissue is transferred from the chylomicron remnants to high density lipoprotein, along with cholesterol. The high density lipoproteins are then taken up by the liver where they are repackaged into very low density lipoproteins and excreted to the plasma. At this stage, α-tocopherol is preferentially incorporated into very low density lipoproteins, possibly through the action of the tocopherol binding protein. Half of the very low density lipoproteins are subsequently degraded by lipoprotein lipase and hepatic triglyceride lipase to form low density lipoproteins.
The LDL particle is the major transport route of cholesterol to tissues, and LDL is taken up by a receptor mediated process in tissues possessing a high cholesterol requirement. Tissues such as the adrenal glands, adipose tissue, liver, intestine, testes and ovaries may receive high concentrations of vitamin E in this way therefore. The oxidation of the low density lipoprotein is now implicated in the development of atherosclerosis and cardiovascular disease. Vitamin E may protect low density lipoprotein from oxidation and therefore be a beneficial cardioprotective agent. Adipose tissue is the primary store of vitamin E, and the removal of vitamin E from adipose tissue may be an important mechanism for maintaining vitamin E plasma levels during time of insufficient intake. There might be an active mechanism for removal of this vitamin E because during depletion studies, other stores of vitamin E are not catabolised.
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