| High selenium diet protects against TNBS-induced acute inflammation, mitochondrial dysfunction, and secondary necrosis in rat colon. | |
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MedLine Citation:
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PMID: 17936198 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: We studied the protective effects of selenium in a rat model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis to elucidate a possible mechanism of action. METHOD: Rats were supplemented with sodium selenite for 21 d with a normal selenium diet (0.02 microg/g body weight), an intermediate selenium diet (ISD; 0.3 microg/g body weight), or a high selenium diet (HSD; 2 microg/g body weight). On day 22, colitis was induced with TNBS. Rats were sacrificed after 24 h and colonic tissue was removed for evaluation. RESULTS: Selenium supplementation (HSD) resulted in a significant increase in selenium in colonic tissue. Morphologically, the HSD resulted in the preservation of tissue architecture and attenuated neutrophil infiltration; no vasculitis or necrosis was detected. Biochemically, the HSD decreased tissue myeloperoxidase activity and protected the mitochondria in the colon of TNBS-treated animals as evaluated by preserving tissue oxygen consumption, mitochondrial DNA, and expression of cytochrome c. The HSD increased levels of nuclear respiratory factor-1 and mitochondrial transcription factor-A in normal colon tissue and under inflammatory conditions. The ISD resulted in only a minor protective effect. CONCLUSION: The results indicate that tissue damage in TNBS-induced colitis is accompanied by the arrest of mitochondrial respiration, loss of mitochondrial DNA, and the expression of nuclear-encoded mitochondrial proteins. Selenium effectively protects colon mitochondria by upregulation of the expression of mitochondrial transcription factors nuclear respiratory factor-1 and mitochondrial transcription factor-A. Selenium prevented inflammatory and necrotic changes after induction of colitis. Selenium in a high dose is therefore a potential therapeutic agent in inflammatory bowel disease. |
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Authors:
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Oren Tirosh; Eran Levy; Ram Reifen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Nutrition (Burbank, Los Angeles County, Calif.) Volume: 23 ISSN: 0899-9007 ISO Abbreviation: Nutrition Publication Date: 2007 Nov-Dec |
Date Detail:
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Created Date: 2007-10-15 Completed Date: 2008-02-01 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8802712 Medline TA: Nutrition Country: United States |
Other Details:
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Languages: eng Pagination: 878-86 Citation Subset: IM |
Affiliation:
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The School of Nutritional Sciences, Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot, Israel. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Colitis / chemically induced, enzymology, pathology, prevention & control* Colon / pathology* DNA, Mitochondrial / drug effects, metabolism* Dietary Supplements Dose-Response Relationship, Drug Gene Expression Regulation Male Mitochondria / drug effects*, physiology Oxygen Consumption Rats Rats, Sprague-Dawley Selenium / administration & dosage*, metabolism Trinitrobenzenesulfonic Acid / toxicity |
| Chemical | |
Reg. No./Substance:
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0/DNA, Mitochondrial; 2508-19-2/Trinitrobenzenesulfonic Acid; 7782-49-2/Selenium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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