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Antioxidants disease/disorder effects

The interrelations between vitamin E and selenium in cattle and sheep are undoubtedly as complex as they are in other species. It seems reasonable to state that vitamin E, in combatting the toxicity of unsaturated fat, acts as an antioxidant, for its effect can be duplicated by many other antioxidants and redox dyestuffs. Similarly it is indisputable that selenium is a dietar essential for ruminants and that its absence from their diet results in muscular disease. Both unsaturated fat excess and selenium deficiency must produce primary disturbances in the muscle cells. These disturbances need not be common to both, for muscle reacts similarly to a variety of biochemical insult. In the presence of selenium and the absence of unsaturated fat, vitamin E requirements of ruminants appear to be extremely small. The failure to produce reproductive disorders in ruminants by experimental vitamin E deficiency, and the failure to produce muscular disease on fat-free diets deficient in vitamin E but likely to have been adequate in selenium content is evidence of this contention. How vitamin E acts in preventing muscular disease due to selenium deficiency, however, is not known, and this aspect needs elucidation. [Pg.641]

Ascorbic acid also forms soluble chelate complexes with iron (142—145). It seems ascorbic acid has no effect on high iron levels found in people with iron overload (146). It is well known, in fact, that ascorbic acid in the presence of iron can exhibit either prooxidant or antioxidant effects, depending on the concentration used (147). The combination of citric acid and ascorbic acid may enhance the iron load in aging populations. Iron overload may be the most important common etiologic factor in the development of heart disease, cancer, diabetes, osteoporosis, arthritis, and possibly other disorders. The synergistic combination of citric acid and ascorbic acid needs further study, particularly because the iron overload produced may be correctable (147). [Pg.22]

Asai et al. (1999) determined that phospholipid hydroperoxides (PLOOH) are key products for oxidative injury in membranous phospholipid layers in the plasma, red blood cells (RBC), and liver of mice. The formation and accumulation of PLOOH have been confirmed in several cellular disorders, various diseases, and in aging. A lower PLOOH level was found in RBC of the spice-extract-fed mice (65 to 74% of the nonsupplemented control mice). The liver lipid peroxidizability induced with Fe2+/ascorbic acid was effectively suppressed in mice by dietary supplementation with the turmeric and capsicum extracts. Although no difference in the plasma lipids was observed, the liver triacylglycerol concentration of the turmeric-extract-fed mice was markedly reduced to half of the level in the control mice. These findings suggest that these spice extracts could act antioxidatively in vivo by food supplementation, and that the turmeric extract has the ability to prevent the deposition of triacylglycerols in the liver. [Pg.237]

Given the phytochemical complexity of figs, this fruit is a treasure trove for basic research. Currently, there are potential applications for figs and its extracts against cancer, microbial and viral infections, pain, skin diseases, sun exposure, cardiovascular and digestive disorders, metabolic syndrome, and nutritional deficiencies, to cite only a partial list. As many of these diseases could have a common origin from inflammatory mechanisms, recent research on the potential health properties of figs has focused on their antioxidant and anti-inflammatory effects. [Pg.52]

The scientific community has been discussing for quite some time now the relationship between oxidative stress, defined as the imbalance between oxidant and antioxidants [45], and the health-disease status. An impressive amount of information available in the literature deals with the effects of the classic antioxidants, ascorbic acid, a-tocopherol, and jS-carotene in a huge series of pathophysiological situations in experimental animals and humans. Concerning the effects of the classic antioxidants on mitochondrial function in situations of oxidative stress, the information is not so vast and most of the time it is not conclusive. However, substantial progress has been made in the description of the mitochondrial alterations in neurodegenerative diseases and in the a-tocopherol effects,both as prevention and as treatment [46]. We will briefly review some reports related to vitamin E and mitochondrial dysfunction in oxidative metaboHc disorders and in the neurodegenerative Alzheimer s and Parkinson s diseases. [Pg.226]


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See also in sourсe #XX -- [ Pg.29 ]




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Disease effects

Disorder effects

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