| Cellular antioxidant properties of human natural killer enhancing factor B. | |
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MedLine Citation:
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PMID: 9161849 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The protein, NKEF (natural killer enhancing factor), has been identified as a member of an antioxidant family of proteins capable of protecting against protein oxidation in cell-free assay systems. The mechanism of action for this family of proteins appears to involve scavenging or suppressing formation of protein thiyl radicals. In the present study we investigated the antioxidant protective properties of the NKEF-B protein overexpressed in an endothelial cell line (ECV304). Nkef-B-transfected cells displayed significantly lower levels of reactive oxygen species (ROS) compared with control or vector-transfected cells. Tert-Butylhydroperoxide-induced ROS was 15% lower in nkef-B-transfected cells and cytotoxicity was slightly, though not significantly, lower. NKEF-B had no effect on ROS induced by menadione or xanthine plus xanthine oxidase. NKEF-B overexpression resulted in slightly (approximately 10%) lower levels of cellular glutathione (GSH) and had no effect on rate or extent of GSH depletion following either diethylmaleate (DEM) or buthionine sulfoximine (BSO) treatment. Lipid peroxidation, assessed as thiobarbituric acid-reactive substances, was 40% lower in nkef-B-transfected cells compared with vector-only-transfected cells. DEM-induced lipid peroxidation was suppressed by NKEF-B at DEM concentrations of 20 microM to 1 mM. At 10 mM DEM, lipid peroxidation was unaffected by NKEF-B. NKEF-B expression also protected cells against menadione-induced inhibition of [3H]-thymidine uptake. The NKEF-B protein appears most effective in suppressing basal low-level oxidative injury such as that produced during normal metabolism. These results indicate that overexpression of the NKEF-B protein promotes resistance to oxidative stress in this endothelial cell line. |
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Authors:
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T A Sarafian; N Rajper; B Grigorian; A Kim; H Shau |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Free radical research Volume: 26 ISSN: 1071-5762 ISO Abbreviation: Free Radic. Res. Publication Date: 1997 Mar |
Date Detail:
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Created Date: 1997-07-18 Completed Date: 1997-07-18 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9423872 Medline TA: Free Radic Res Country: SWITZERLAND |
Other Details:
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Languages: eng Pagination: 281-9 Citation Subset: IM |
Affiliation:
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Department of Pathology, UCLA 90095, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Antioxidants
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metabolism* Blood Proteins / physiology* Cell Death / physiology Cell Line Dose-Response Relationship, Drug Epithelial Cells Epithelium / drug effects, physiology Fluoresceins / metabolism Glutathione / metabolism Heat-Shock Proteins Humans Maleates / pharmacology Peroxidases Peroxides / pharmacology Peroxiredoxins Reactive Oxygen Species / metabolism* Thiobarbituric Acid Reactive Substances / metabolism Toxins, Biological / pharmacology Transfection Vitamin K / pharmacology tert-Butylhydroperoxide |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Blood Proteins; 0/Fluoresceins; 0/Heat-Shock Proteins; 0/Maleates; 0/Peroxides; 0/Reactive Oxygen Species; 0/Thiobarbituric Acid Reactive Substances; 0/Toxins, Biological; 12001-79-5/Vitamin K; 141-05-9/diethyl maleate; 2044-85-1/diacetyldichlorofluorescein; 70-18-8/Glutathione; 75-91-2/tert-Butylhydroperoxide; EC 1.11.1.-/Peroxidases; EC 1.11.1.15/PRDX2 protein, human; EC 1.11.1.15/Peroxiredoxins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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