Research Accomplishment Reports 2007

Antioxidant Nutrients, Reactive Oxygen Species and Oxidative Stress

C.K. Chow
Department of Human Environmental Sciences

 

Project Description

Vitamin E is the major lipid-soluble chain-breaking antioxidant that prevents free radical-initiated peroxidative tissue damage, and plays a central role in the overall antioxidant defense. The antioxidant property of vitamin E is attributable to its more rapid reaction with peroxy radicals several orders of magnitude faster than with acyl lipids. The free radical scavenging reaction of vitamin E reduces the available superoxide and related reactive oxygen/nitrogen species. However, the mechanism by which vitamin E exerts its protective effect against oxidative tissue damage has yet to be delineated.

Previous studies have shown that dietary vitamin E reduced generation and/or levels of superoxide. As superoxide has potential to release iron from its transport and storage proteins, labile or available form of iron is capable of catalyzing the formation of reactive hydroxyl radicals, in order to understand how vitamin E exerts its antioxidant function, the effect of dietary vitamin E on labile iron pool was studied in rats. One-month-old Sprague-Dawley male and female rats were fed a basal vitamin E-deficient diet supplemented with 0, 20, 200, or 2,000 iu vitamin E/kg diet for 90 days. The levels of labile iron were measured in the liver, kidney, spleen, heart and skeletal muscle. Additionally, the levels of lipid peroxidation products were measured. The results showed that, except for labile iron in the heart of male rats, dietary vitamin E dose-dependently reduced the levels of labile iron and lipid peroxidation products in all tissues of male and female rats. Superoxide and/or hydrogen peroxide has potential to release labile or available form of iron from its protein complexes. Since labile or available form of iron is capable of catalyzing the formation of hydroxyl radicals as well as the decomposition of lipid hydroperoxides to form more free radicals, an increase in labile iron is expected to cause an increase in the levels of oxidation products.

The findings suggest that vitamin E may exert its antioxidant function by attenuating iron release by reducing available superoxide. These data also supports the notion that labile or available form of iron plays an important role in initiating peroxidative damage to membrane lipids and important cellular components.

Impact

Protection against free radical-initiated oxidative damage has long been accepted as the most important biological function proposed for vitamin E. However, the mechanism by which vitamin E exerts its antioxidant function at the tissue level has yet to be delineated. The findings that dietary vitamin E attenuates the levels of labile or reduced iron, which is capable of catalyzing the formation of reactive hydroxyl radicals from superoxide and hydrogen peroxide, provide a rational explanation as to how vitamin E may exerts its antioxidant function at the tissue level.

Publications

Chow, C.K. Grape powder polyphenols and atherosclerosis development. J. Nutr. 136: 2272-2272, 2006.

Chow, C.K. And w. Ibrahim. Dietary vitamin E, but not coenzyme q10, reduces labile iron levels in rat tissues. Metal ions biol. Med. 9: 346-351, 2006.

Chow, C.K. Does potassium-enriched salt or sodium reduction reduce cardiovascular mortality and medical expenses? Am. J. Clin. Nutr. 84: 1552-1553, 2006.

Chow, C.K. Role of vitamin E in cellular antioxidant defense - a new perspective. In new topics in vitamin E research (o.h. Bellock, ed.), nova science publishers, hauppauge, ny, pp. 99-110, 2007.

Chow, C.K. and S.J. Chang. Value or usefulness of the food frequency questionnaire for the assessment of dietary total antioxidant capacity. J. Nutr. 137: 1496-1497, 2007.

L.W. Robertson, I.G. Berberian, T. Borges, l.-C. Chen, C.K. Chow, H.P. Glauert, J. Filser and H. Thomas. Suppression of peroxisomal enzyme activities and cytochrome p4504a isozyme expression by congeneric polybrominated and polychlorinated biphenyls. Ppar res., vol. 2007, article id 15481, 5 pages, 2007.