|
|
|
|
|
|
|
 |
|
|
VITAMIN E
Vitamin E actually refers to a family of moleculces. D-alpha-tocopherol is the most biologically active naturally-occurring form of vitamin E. Vitamin E is a lipid-soluble vitamin (i.e., it dissolves in fat) and one of the most potent antioxidants (free radical 'neutralizers') in the human diet. Vitamin E is typically used as a general health supplement and to reduce one's risk of acquiring chronic disease (e.g., cardiovascular disease, cerebrovascular disease, cancer, Alzheimer's).
Like vitamin C and alpha-lipoic acid, the powerful antioxidant properties of vitamin E may render it useful in the prevention and treatment of oxidative stress, such as is associated with ischemia-reperfusion injury (e.g., as following a heart attack or stroke), severe exercise (e.g., exhaustive distance running), drug toxicity, inflammatory conditions, diabetes, and more. As discussed under product summaries for Essential Fatty acids, unsaturated fatty acids contain one or more double bonds along the length of their carbon chains. These double bonds are sites of high chemical reactivity.
While the chemical reactivity of unsaturated fatty acids is critical to their useful biological properties (e.g., as in the case of essential fatty acids and their metabolites), it also renders the fatty acids susceptible to oxidation. In the absence of sufficient antioxidant protection, this can cause oxidative stress to surrounding cellular structures (e.g., membranes, proteins, DNA). In regards to cellular membranes, for instance, polyunsaturated fatty acid-enriched membranes are at greater risk of oxidative damage. Vitamin E can break the chain of free radical propagation along such structures, thereby preserving cellular integrity and function.
Klein (2002) notes that Vitamin E "especially protects PUFAs within phospholipids of biological membranes and in plasma lipoproteins. As a result, the vitamin E requirement is proportional to the amount of PUFA that is consumed and incorporated into membranes. Iron administration may also increase vitamin E need, because iron catalyzes the oxidation of cellular lipids through generation of free radicals. Iron also interferes with vitamin E absorption by increasing its destruction in the gut. The tocopheroxy radical (formed after reaction of tocopherol with other organic peroxy radicals) prevents further oxidation of lipids. In addition, alpha-tocopherol shows structure-specific effects on several enzyme activities and membrane properties. For example, it down-regulates vascular smooth muscle cell proliferation, decreases protein kinase C activity, suppresses arachidonic acid metabolism via phospholipase A2 inhibition, and enhances the degradation of the enzyme hydroxymethylglutaryl-coenzyme A reductase, which catalyzes the rate-limiting step in cholesterol biosynthesis."
Thus as the intake of unsaturated fatty acids increases, so too should the intake of vitamin E, ideally in combination with other lipid-soluble and water-soluble vitamins. Klein (2002) comments: "Regeneration of tocopherol from the tocopheroxy radical may occur in the presence of ascorbate (vitamin C) or thiols, especially glutathione, as hydrogen donors. Therefore, the vitamin E requirement also depends on the adequacy of other reducing agents, such as vitamin C. It further depends on selenium, which is essential for the activity of glutathione peroxidase. The flux through the cyclic radical pathway may be much larger than the flux through the pathway of degradation."
REFERENCES
Klein (2002). Nutrient Requirements For Preterm Infant Formulas. J Nutr, 132:1395S.
Suggested Doses
100-800 IU per day, with meals.
|
|
|
|
|
|
|
|
|
