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Role of free Radicals

Aging

Aging is a process, which involves the accumulation of changes, which can be attributed to genetic defects, the environment, disease and also the inborn aging process. Many pathological conditions are associated with this process, including the development of cataracts, diabetes and macular degeneration. Ageing is thought to be caused by free radical reactions, generated in the mitochondria, which accumulate with age. Free radicals cause the progressive oxidation of protein and lipid components in the cell membranes and also activate phospholipases, proteases and endonucleases. Increased lipid peroxidation has been implicated in the ageing process followed by an induction of detoxification enzymes. Wrinkle formation in the skin has also been attributed to long-term exposure to oxidative damage light, resulting in the production of free radicals.

Some studies have shown that free radical chain reactions are associated with the aging process. These chain reactions may be decreased by increasing the intake of components, which enhances antioxidant capacity, e.g. fruits and vegetables, or by supplementing the diet with antioxidants, e.g. vitamin E, C and ß-carotene. The skin has developed complex defense mechanism, to combat long-term exposure to ROS, such as antioxidant enzymes and low molecular weight antioxidants. The activities of antioxidant enzymes in wrinkles is decreased significantly through oxidative stress and aging. As a result of the research in this field many cosmetic companies now add antioxidant components such as vitamin E to their products to protect the skin from free radical damage.

References

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  2. Tanida T. Ueta E. Tobiume A. Hamada T. Rao F. Osaki T. Influence of aging on candidal growth and adhesion regulatory agents in saliva. Journal of Oral Pathology & Medicine. 30(6):328-35, 2001

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  4. Ghezzo-Schoneich E. Esch SW. Sharov VS. Schoneich C. Biological aging does not lead to the accumulation of oxidized Cu,Zn-superoxide dismutase in the liver of F344 rats. Free Radical Biology & Medicine. 30(8):858-64, 2001

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  6. Adachi T. Yamamoto M. Hara H. Masuda K. Mitsui N. Oh-ishi T. Okazaki M. Extracellular-superoxide dismutase in cerebrospinal fluid from infants/children. Clinica Chimica Acta. 308(1-2):191-3, 2001

  7. Hall DM. Sattler GL. Sattler CA. Zhang HJ. Oberley LW. Pitot HC. Kregel KC. Aging lowers steady-state antioxidant enzyme and stress protein expression in primary hepatocytes. Journals of Gerontology Series A-Biological Sciences & Medical Sciences. 56(6):B259-67, 2001

  8. Moon SK. Thompson LJ. Madamanchi N. Ballinger S. Papaconstantinou J. Horaist C. Runge MS. Patterson C. Aging, oxidative responses, and proliferative capacity in cultured mouse aortic smooth muscle cells. American Journal of Physiology - Heart & Circulatory Physiology. 280(6):H2779-88, 2001

  9. Tanguy S. Boucher F. Toufektsian MC. Besse S. de Leiris J. Aging exacerbates hydrogen peroxide-induced alteration of vascular reactivity in rats. Antioxidants & Redox Signaling. 2(2):363-8, 2000

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  11. Hamilton CA. Brosnan MJ. McIntyre M. Graham D. Dominiczak AF. Superoxide excess in hypertension and aging: a common cause of endothelial dysfunction. Hypertension. 37(2 Part 2):529-34, 2001

  12. Ruetten H. Zabel U. Linz W. Schmidt HH. Downregulation of soluble guanylyl cyclase in young and aging spontaneously hypertensive rats. Circulation Research. 85(6):534-41, 1999

  13. Imre S. Csornai M. Balazs M. High sensitivity to autoxidation in neonatal calf erythrocytes: possible mechanism of accelerated cell aging. Mechanisms of Ageing & Development. 122(1):69-76, 2001

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