Document Detail


Cellular antioxidant properties of human natural killer enhancing factor B.
MedLine Citation:
PMID:  9161849     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
T A Sarafian; N Rajper; B Grigorian; A Kim; H Shau
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Free radical research     Volume:  26     ISSN:  1071-5762     ISO Abbreviation:  Free Radic. Res.     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-07-18     Completed Date:  1997-07-18     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9423872     Medline TA:  Free Radic Res     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  281-9     Citation Subset:  IM    
Affiliation:
Department of Pathology, UCLA 90095, USA.
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MeSH Terms
Descriptor/Qualifier:
Antioxidants / 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:
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

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