Source:http://linkedlifedata.com/resource/pubmed/id/17704323
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2007-8-20
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pubmed:abstractText |
Given the increasing population of long-term cancer survivors, the need to mitigate or treat late effects has emerged as a primary area of radiation biology research. Once thought to be irreversible, radiation-induced late effects are now viewed as dynamic multicellular interactions between multiple cell types within a particular program that can be modulated. The molecular, cellular and biochemical pathways responsible for radiation-induced late morbidity remain ill-defined. This review provides data in support of the hypothesis that these late effects are driven, in part, by a chronic oxidative stress. Irradiating late responding normal tissues leads to chronic increases in reactive oxygen/reactive nitrogen oxide species that serve as intracellular signaling species to alter cell function/phenotype, resulting in chronic inflammation, organ dysfunction, and ultimate fibrosis and/or necrosis. Furthermore, we hypothesize that the effectiveness of renin-angiotensin system blockers in preventing or mitigating the severity of radiation-induced late effects reflects, in part, inhibition of reactive oxygen species generation and the resultant chronic oxidative stress. These findings provide a robust rationale for anti-inflammatory-based interventional therapies in the treatment of late normal tissue injury.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1748-880X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
80 Spec No 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S23-31
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17704323-Angiotensin II,
pubmed-meshheading:17704323-Animals,
pubmed-meshheading:17704323-Humans,
pubmed-meshheading:17704323-Inflammation,
pubmed-meshheading:17704323-Oxidative Stress,
pubmed-meshheading:17704323-Radiation Injuries,
pubmed-meshheading:17704323-Reactive Nitrogen Species,
pubmed-meshheading:17704323-Reactive Oxygen Species,
pubmed-meshheading:17704323-Signal Transduction
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pubmed:year |
2007
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pubmed:articleTitle |
Oxidative damage pathways in relation to normal tissue injury.
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pubmed:affiliation |
Department of Radiation Oncology, Brain Tumor Center of Excellence, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, N.I.H., Extramural
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