| Isoforms of vitamin E differentially regulate inflammation. | |
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MedLine Citation:
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PMID: 20923401 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Vitamin E regulation of disease has been extensively studied in humans, animal models and cell systems. Most of these studies focus on the α-tocopherol isoform of vitamin E. These reports indicate contradictory outcomes for anti-inflammatory functions of the α-tocopherol isoform of vitamin E, especially with regards to clinical studies of asthma and atherosclerosis. These seemingly disparate clinical results are consistent with recently reported unrecognized properties of isoforms of vitamin E. Recently, it has been reported that physiological levels of purified natural forms of vitamin E have opposing regulatory functions during inflammation. These opposing regulatory functions by physiological levels of vitamin E isoforms impact interpretations of previous studies on vitamin E. Moreover, additional recent studies also indicate that the effects of vitamin E isoforms on inflammation are only partially reversible using physiological levels of a vitamin E isoform with opposing immunoregulatory function. Thus, this further influences interpretations of previous studies with vitamin E in which there was inflammation and substantial vitamin E isoforms present before the initiation of the study. In summary, this review will discuss regulation of inflammation by vitamin E, including alternative interpretations of previous studies in the literature with regards to vitamin E isoforms. |
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Authors:
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Joan M Cook-Mills; Christine A McCary |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Endocrine, metabolic & immune disorders drug targets Volume: 10 ISSN: 2212-3873 ISO Abbreviation: Endocr Metab Immune Disord Drug Targets Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2011-01-10 Completed Date: 2011-04-18 Revised Date: 2012-04-19 |
Medline Journal Info:
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Nlm Unique ID: 101269157 Medline TA: Endocr Metab Immune Disord Drug Targets Country: United Arab Emirates |
Other Details:
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Languages: eng Pagination: 348-66 Citation Subset: IM |
Affiliation:
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Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. j-cook-mills@northwestern.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Inflammatory Agents / chemistry, therapeutic use* Antioxidants / therapeutic use Disease Models, Animal Humans Inflammation / immunology, prevention & control* Inflammation Mediators / metabolism Molecular Structure Reactive Oxygen Species / metabolism Signal Transduction / drug effects Structure-Activity Relationship Vascular Cell Adhesion Molecule-1 / drug effects, metabolism Vitamin E / chemistry, therapeutic use* |
| Grant Support | |
ID/Acronym/Agency:
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AT004837/AT/NCCAM NIH HHS; HL069428/HL/NHLBI NIH HHS; R01 AT004837-01/AT/NCCAM NIH HHS; R01 AT004837-02/AT/NCCAM NIH HHS; R01 AT004837-03/AT/NCCAM NIH HHS; R01 AT004837-04/AT/NCCAM NIH HHS; R01 HL069428-01A2/HL/NHLBI NIH HHS; R01 HL069428-02/HL/NHLBI NIH HHS; R01 HL069428-03/HL/NHLBI NIH HHS; R01 HL069428-04/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Antioxidants; 0/Inflammation Mediators; 0/Reactive Oxygen Species; 0/Vascular Cell Adhesion Molecule-1; 1406-18-4/Vitamin E |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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