By Tapan K Basu, N Temple, Manohar L. Garg
Antioxidants play a tremendous function within the development of significant human degenerative illnesses and stipulations. This publication covers antioxidants and their mechanisms of motion; their function in an entire array of stipulations together with heart ailment, malignant disorder, diabetes, cataracts, respiration disorder, cystic fibrosis, cognitive services, and getting older; their signs for oxidative pressure; and patron concerns. nearly all of chapters were constructed from papers provided on the sixth international Congress in medical nutrients, held in Banff, Canada, July 1997.
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Extra resources for Antioxidants in Human Health and Disease
Ford, I. G. (1995) Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. New England Journal of Medicine 333, 1301–1307. , Svensson, I. T. (1990) Hydrogen peroxide production by liver mitochondria in different species. Mechanisms of Aging and Development 53, 209–215. C. B. (1992) Glutathione redox cycle enzymes and selenium in severe rheumatoid arthritis: lack of antioxidative response to selenium supplementation in polymorphonuclear leucocytes. Annals of Rheumatic Disease 51, 1044–1049.
1989). In addition, plasma devoid of ascorbate but no other endogenous antioxidants, such as ␣-tocopherol, was found to be extremely susceptible to lipid peroxidative damage. Animal studies have reported that marginal ascorbate deficiency induced by diet leads to myocardial injury as evidenced by lipid peroxidation; this damage was prevented by ascorbic acid supplementation. Such observations have also been made in human studies. Thus, elderly subjects receiving 400 mg of ascorbic acid daily for 1 year, experienced a 13% decrease in serum peroxide levels.
The pathological consequences of lipid free-radical and peroxide productions have been well documented, and they have been implicated for their role in atherogenesis (Steinberg, 1987). It has been suggested that the concentrations of lipid peroxides in the plasma correlate well with the severity of atherosclerotic lesions. It is believed that these reactive substances eventually react with apolipoprotein B (apo-B), the sole protein component of LDL, and promote its oxidation. , 1989). , 1991). It has, thus, a greater density and increased negative changes compared to native LDL.