Author(s): Burton GW, Burton GW
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Abstract There is a growing body of evidence implicating free radicals in a wide variety of medical diseases and conditions, especially the diseases of ageing, such as cancer and cardiovascular disease, which appear to be ultimate expressions of long-term, cumulative and sustained cellular damage. Vitamin E is an excellent lipid-soluble, chain-breaking antioxidant in the presence of other co-operative antioxidants such as vitamin C or ubiquinol, but it can act as a pro-oxidant in their absence. Epidemiological findings and animal studies support the belief that vitamin E is protective against cardiovascular disease and possibly cancer. The wide range of symptoms associated with vitamin E deficiency is consistent with a loss of antioxidant protection in those long-lived cells in which there is sufficient opportunity for accumulation of free radical damage. The cellular damage is proposed to arise from the generation of free radicals during normal aerobic metabolism. Some susceptible tissues may have enhanced levels of radicals that are produced, for example, by the action of cytochrome P-450 enzymes in steroidogenic tissues, or by the generation of NO in neural tissues.
This article was published in Proc Nutr Soc
and referenced in Journal of AIDS & Clinical Research