Source:http://linkedlifedata.com/resource/pubmed/id/12205044
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2002-9-2
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pubmed:abstractText |
Tumor necrosis factor a (TNF-alpha) is a pleiotropic cytokine involved in several diseases. Various effects of TNF-alpha are mediated by the induction of a cellular state consistent with oxidative stress. Glutathione (GSH) is a major redox-buffer of eukaryotic cells and is important in the defense against oxidative stress. We hypothesized that persistent TNF-alpha secretion could induce oxidative stress through modulation of GSH metabolism. This hypothesis was examined in a transgenic mouse model with low, persistent expression of human TNF-alpha in the T cell compartment. Major findings were i) marked tissue-specific changes in GSH redox status and GSH regulating enzymes, with the most pronounced changes in liver; ii) moderate changes in GSH metabolism and up-regulation of GSH-regulating enzymes were observed in lung and kidney from transgenic mice; and iii) liver, lung and kidney from transgenic mice had decreased levels of total glutathione, whereas splenic CD4+ and CD8+ T cells had a marked increase in oxidized glutathione as the major change. Oxidative stress induced by persistent low-grade exposure to TNF-alpha in transgenic mice appears to involve marked organ-specific alterations in glutathione redox status and glutathione-regulating enzymes with the most pronounced changes in the liver. These mice constitute a useful model for immunodeficiency syndromes and chronic inflammatory diseases involving pathogenic interaction between TNF-alpha and oxidative stress.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1530-6860
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1450-2
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:12205044-Animals,
pubmed-meshheading:12205044-Antioxidants,
pubmed-meshheading:12205044-Glutathione,
pubmed-meshheading:12205044-Humans,
pubmed-meshheading:12205044-Kidney,
pubmed-meshheading:12205044-Liver,
pubmed-meshheading:12205044-Lung,
pubmed-meshheading:12205044-Mice,
pubmed-meshheading:12205044-Mice, Transgenic,
pubmed-meshheading:12205044-Organ Specificity,
pubmed-meshheading:12205044-Oxidation-Reduction,
pubmed-meshheading:12205044-Oxidative Stress,
pubmed-meshheading:12205044-T-Lymphocytes,
pubmed-meshheading:12205044-Tumor Necrosis Factor-alpha
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pubmed:year |
2002
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pubmed:articleTitle |
Human TNF-alpha in transgenic mice induces differential changes in redox status and glutathione-regulating enzymes.
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pubmed:affiliation |
Biotechnology Centre of Oslo, University of Oslo, PB 1125 Blindern, 0317 Oslo, Norway.
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pubmed:publicationType |
Journal Article
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