Aging at the Molecular Level by Nicolle Sitte, Thomas von Zglinicki (auth.), Thomas von

By Nicolle Sitte, Thomas von Zglinicki (auth.), Thomas von Zglinicki (eds.)

During the final forty years, the learn of the organic foundation of getting older has stepped forward drastically, and it has now turn into an self reliant and first rate box of analysis and learn. the fundamental reason for getting older is molecular harm that slowly overwhelms mobile and organismic safety, fix and upkeep platforms. lately, a wealth of hugely refined study has remodeled this concept from a reputable speculation not just to an immense idea, yet primarily to accredited wisdom. getting older on the Molecular point examines the foremost parts during this transformation.
Bringing jointly contributions from a global staff of authors, this quantity could be of curiosity to graduates and postgraduates within the fields of drugs and nursing, researchers of other points of biogerontology and people within the pharmaceutical, cosmeceutical, nutraceutical and health-care industry.

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An adequate pool of glutathione as a protectant is essential to prevent this increase in sulfhydryl oxidation. However, changes in the glutathione redox status during the aging process indicate that there is only a limited potential for regeneration of oxidized protein sulfhydryls left [reviewed in ref. 11]. 40 NICOLLE SITTE Accumulation and degradation of oxidized proteins during aging The carbonyl content of tissues from various species has been shown to increase dramatically in the last third of life span, reaching such a level that on average one out of every three protein molecules carries the modification [34].

DNA repair disorders are often associated with elevated cancer frequencies and heterozygosity of defects in mismatch repair genes are known to be autosomal dominant in promoting nonpolyposis colon cancer in humans. The role of DNA repair in the prevention of aging is partly supported by repair genes being mutated in patients with premature aging syndromes such as Werner syndrome (WRN, RecQ helicase) and Cockayne syndrome [see Chapter 5, this volume]. Perhaps the best recent evidence for the role of oxidative DNA repair in the prevention of aging comes from the study of mouse models with targeted defects in XPD and XPA.

In: Cutler RG, Packer L, Bertram J, MoriA, eds. Oxidative Stress and Aging. Basel, Switzerland: Birkhauser Verlag, pp. 141-9. 28. Levine RL, Williams JA, Stadtman ER, Shacter E (1994). Carbonyl assays for determination of oxidatively modified proteins. Methods Enzyrnol. 233: 346-57. 29. Stadtman ER (1997). Free radical mediated oxidation of proteins. In: Ozben T, ed. Free Radics, Oxidative Stress, and Antioxidants. Pathological and Physiological Significance. NATO ASI Series, Series A: Life Sciences, 296.

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