| Cell responses to oxidative stressors. | |
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MedLine Citation:
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PMID: 20166986 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Stress is a stimulus or a succession of stimuli tending to disrupt the homeostasis of an organism. An organism is consisting of a multitude of cells that singly undergo the effects of external factors that disturb or upset their homeostatic regulation. Stimuli acting as potential stressors are numerous, and include physical agents (ionizing radiation), non-physiological oxygen levels (hypoxia, hyperoxia) and chemotherapeutics. Lastly, also senescence, a physiological process occurring in all organisms, can be considered as a potential stressor. The cell response to multiple oxidative stresses involves mitochondria, since these organelles represent the major source of Reactive Oxygen Species (ROS) that drive the occurrence of pathological conditions and ageing by activating specific signalling pathways. Nevertheless, under physiological conditions the cells are able to exert an antioxidant response which, controlling ROS/Reactive Nitrogen Species (RNS) homeostasis, is involved in mediating cell differentiation, proliferation and migration. Thus, this review focuses the attention to the role played by mitochondria in the physiological and non-physiological signalling responses of eukaryotic cells to some oxidative stresses, in order to identify potential therapeutic targets to counteract oxidative stress effects and mitochondrial-related pathologies. |
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Authors:
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Amelia Cataldi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Current pharmaceutical design Volume: 16 ISSN: 1873-4286 ISO Abbreviation: Curr. Pharm. Des. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-05-27 Completed Date: 2010-08-20 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9602487 Medline TA: Curr Pharm Des Country: Netherlands |
Other Details:
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Languages: eng Pagination: 1387-95 Citation Subset: IM |
Affiliation:
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Dipartimento di Biomorfologia, Cattedra di Anatomia Umana, Facoltà di Farmacia, Università G. d'Annunzio, Chieti-Pescara, Via dei Vestini, 6, 66100, Chieti - Italy. cataldi@unich.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antineoplastic Agents / pharmacology Cell Aging / drug effects, radiation effects Cyclic AMP / metabolism Eukaryotic Cells / drug effects, enzymology, metabolism, radiation effects Homeostasis / drug effects*, radiation effects* Humans Hypoxia-Inducible Factor 1 / metabolism Mitochondria / drug effects*, metabolism, radiation effects* Nitric Oxide / metabolism Oxidative Stress* / drug effects, radiation effects Oxygen Consumption / drug effects, radiation effects Protein Kinase C / metabolism Radiation, Ionizing Reactive Oxygen Species / metabolism Signal Transduction / drug effects, radiation effects Telomerase / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Antineoplastic Agents; 0/Hypoxia-Inducible Factor 1; 0/Reactive Oxygen Species; 10102-43-9/Nitric Oxide; 60-92-4/Cyclic AMP; EC 2.7.11.13/Protein Kinase C; EC 2.7.7.49/Telomerase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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