Dietary antioxidants modulation of aging and immune-endothelial cell interaction.
Oxidative damage by free radicals, which is the basis for the free radical theory of aging, has been well investigated within the context of oxidant/antioxidant balance. Age-associated disorders are believed to be associated with the time-dependent shift in the antioxidant/prooxidant balance in favor of oxidative stress. In this brief review, the importance of dietary antioxidant intervention on longevity and age-associated changes in bodily functions and diseases are discussed. Evidence has indicated that increasing the endogenous antioxidants defense system and modulation of free radical production by dietary restrictions contribute to increased longevity in animal models. Thus, increasing dietary intake of antioxidants is believed to increase longevity. Earlier studies have shown some increase in median life span in animal models. It was found that supplementing middle-aged (18 months) C57/BL mice with various antioxidants (vitamin E, glutathione, melatonin, and strawberry extract) had no effect on longevity as measured by the average age of death. Therefore, dietary antioxidant supplementation seems unlikely to increase longevity when begun in middle age; supplementation started in early life might be more effective. However, in middle-aged mice, vitamin E was effective in reducing lung viral titer when animals were exposed to influenza virus. Vitamin E supplementation improves cell-mediated immunity in mice and in humans. In addition to modulating the oxidation of low-density lipoproteins, vitamin E can modulate immune/endothelial cells interactions, thus reducing the risk of cardiovascular disease (CVD), a major cause of morbidity and mortality in elderly. Thus, antioxidants such as vitamin E from food sources or supplements appear to be promising for successful aging by improving immune function, and reducing the risk of several age-associated chronic diseases, such as CVD.
Meydani
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Vascular Biology Program, JM USDA-Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA. meydani_vbl@hnrc.tufts.edu
D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D004032:Diet; D004730:Endothelium, Vascular / Q000378:metabolism*; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology*; D008136:Longevity / Q000502:physiology*; D051379:Mice; D018384:Oxidative Stress
D000975:Antioxidants