Oxidative Stress, Poly(ADP)Ribosylation and Aging: In Vitro Studies on Lymphocytes from Normal and Down’s Syndrome Subjects of Different Age and from Patients with Alzheimer’s Dementia
Free radicals are formed in the body as a consequence of aerobic metabolism. Cells have developed a variety of antioxidant systems, that include classical antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and catalase) as well as nonenzymatic oxy-radicals scavengers (vitamin E, urea, ß-carotene and some more recently described substances such as carnosine) (1). However, a certain fraction of active oxygen species escapes the cellular defence and may cause transient or permanent damage to cellular components. According to one of the most interesting theory of aging is the “free radical theory of aging”, proposed by D. Harman (2) more than thirty years ago, where oxidative damage has been suggested as a major cause of aging. One of the prediction of this theory is an age-related decrease of the efficiency of antioxidant defence mechanisms.
KeywordsElectron Spin Resonance Xanthine Oxidase Peripheral Blood Lymphocyte Spin Trapping Free Radical Theory
Unable to display preview. Download preview PDF.
- 4).S. Shall, ADP-ribosylation of proteins: a ubiquitous cellular control mechanism. In: Advances in post-translational modifications of proteins and aging, V. Zappia, P.Galletti, R.Porta and F. Wold eds, Plenum Press, NY 1988.Google Scholar
- 7.C. Franceschi, F. Licastro, M. Chiricolo, M. Zannotti, and M. Masi, Premature senility in Down’s syndrome: a model for and an approach to the molecular genetic of the ageing process. In: Immunoregulation in Aging, A. Facchini, J.J. Harman, and G. Labó, Eurage, Rijswijk (1986).Google Scholar