Cellular responses to reactive oxygen species-induced DNA damage and aging
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Catharina Bertram
Abstract
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.
©2008 by Walter de Gruyter Berlin New York
Artikel in diesem Heft
- Highlight: Oxidative Stress and Senescence
- Regulation of proteasome-mediated protein degradation during oxidative stress and aging
- Cellular responses to reactive oxygen species-induced DNA damage and aging
- Sirt1 protects the heart from aging and stress
- Klotho as a regulator of oxidative stress and senescence
- Posttranscriptional gene regulation by RNA-binding proteins during oxidative stress: implications for cellular senescence
- Potential biomarkers of ageing
- Increased molecular damage and heterogeneity as the basis of aging
- Modulation of longevity-associated genes by estrogens or phytoestrogens
- FoxO transcription factors in oxidative stress response and ageing – a new fork on the way to longevity?
- Studies on the expression of 6S RNA from E. coli: involvement of regulators important for stress and growth adaptation
- New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.
- Regulation of the expression of components of the exocytotic machinery of insulin-secreting cells by microRNAs
- Kinetic properties of cathepsin D and BACE 1 indicate the need to search for additional β-secretase candidate(s)
Artikel in diesem Heft
- Highlight: Oxidative Stress and Senescence
- Regulation of proteasome-mediated protein degradation during oxidative stress and aging
- Cellular responses to reactive oxygen species-induced DNA damage and aging
- Sirt1 protects the heart from aging and stress
- Klotho as a regulator of oxidative stress and senescence
- Posttranscriptional gene regulation by RNA-binding proteins during oxidative stress: implications for cellular senescence
- Potential biomarkers of ageing
- Increased molecular damage and heterogeneity as the basis of aging
- Modulation of longevity-associated genes by estrogens or phytoestrogens
- FoxO transcription factors in oxidative stress response and ageing – a new fork on the way to longevity?
- Studies on the expression of 6S RNA from E. coli: involvement of regulators important for stress and growth adaptation
- New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.
- Regulation of the expression of components of the exocytotic machinery of insulin-secreting cells by microRNAs
- Kinetic properties of cathepsin D and BACE 1 indicate the need to search for additional β-secretase candidate(s)
