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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Ludwig, Stephan / Sies, Helmut / Turk, Boris / Wittinghofer, Alfred

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Cellular responses to reactive oxygen species-induced DNA damage and aging

Catharina Bertram1 / Ralf Hass2

1Department of Gynecology (OE 6411), Medical School Hannover, D-30625 Hannover, Germany

2Department of Gynecology (OE 6411), Medical School Hannover, D-30625 Hannover, Germany

Corresponding author

Citation Information: Biological Chemistry. Volume 389, Issue 3, Pages 211–220, ISSN (Online) 14374315, ISSN (Print) 14316730, DOI: 10.1515/BC.2008.031, March 2008

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Oxidative stress in cells and tissues can occur during pathophysiological developments, e.g., during inflammatory and allergic diseases or during ischemic or toxic and hyperglycemic conditions via the generation of reactive oxygen species (ROS). Moreover, ROS can be generated by radiation (UV, X-rays) and pharmacologically, e.g., by anthracyclins as chemotherapeutic compounds for treatment of a variety of tumors to induce ‘stress or aberrant signaling-inducing senescence’ (STASIS). Although STASIS is distinguished from intracellular replicative senescence, a variety of cellular mechanisms appear similar in both aging pathways. It is generally accepted that oxidative stress and ROS eventually cause DNA damage, whereby insufficient cellular repair mechanisms may contribute to premature aging and apoptosis. Conversely, ROS-induced imbalances of the signaling pathways for metabolic protein turnover may also result in opposite effects to recruit malfunctioning aberrant proteins and compounds that trigger tumorigenic processes. Consequently, DNA damage plays a role in the development of carcinogenesis, but is also associated with an aging process in cells and organisms.

Keywords: antioxidant defense mechanisms; poly(ADP)-ribose polymerase (PARP); rejuvenation; replicative senescence; retrodifferentiation; stress or aberrant signaling-inducing senescence (STASIS)

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