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Summary
Damage of molecules as a consequence of oxidative stress has been implicated in the pathogenesis of chronic diseases related to aging. Diet is a key environmental factor affecting the incidence of many chronic diseases. Antioxidant substances in diet enhance the DNA, lipid and protein protection by increasing the scavenging of free radicals. Products of oxidative damage of DNA (DNA strand breaks with oxidized purines or oxidized pyrimidines), lipids (conjugated dienes of fatty acids) and proteins (carbonyls) in relation to nutrition (vegetarian diet vs. non-vegetarian, traditional mixed diet) were measured in young women aged 20-30 years (46 vegetarians, 48 non-vegetarians) vs. older women aged 60-70 years (33 vegetarians, 34 non-vegetarians). In young subjects, no differences in values of oxidative damage as well as plasma values of antioxidative vitamins (C,β-carotene) were observed between vegetarian and non-vegetarian groups. In older vegetarian group significantly reduced values of DNA breaks with oxidized purines, DNA breaks with oxidized pyrimidines and lipid peroxidation and on the other hand, significantly increased plasma values of vitamin C and β-carotene were found compared to the respective non-vegetarian group. Significant age dependences of measured parameters (increase in all oxidative damage products and decrease in plasma vitamin concentrations in older women) were noted only in non-vegetarians. Vegetarian values of older women vs. young women were similar or non-significantly changed. The results suggest that increase of oxidative damage in aging may be prevented by vegetarian nutrition.
Key words
Oxidative damage * Nutrition * Antioxidative vitamins * Age
Oxidative stress has been implicated in the pathogenesis of chronic diseases related to aging such as cancer and cardiovascular disease (Benzie 2000). It was proposed 50 years ago that free radicals are the major factor involved in the aging process (Harman 1956). The main idea was that aging is caused by the accumulation of free radical-elicited oxidative damage to various biological molecules in tissue cells. Miquel (1991) provided first experimental support to this theory in early years by showing that oxidative damage to mitochondrial DNA and lipofuscin pigment formation in animal tissues are concurrently increased during aging. This "mitochondrial theory of aging" emphasized that enhanced production of reactive oxygen species and accumulation of mitochondrial DNA mutations are a contributory factor to human aging (Linnane et al. 1989).
Evidence...