Document Detail


Visualization of labile zinc and its role in apoptosis of primary airway epithelial cells and cell lines.
MedLine Citation:
PMID:  11076807     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The respiratory epithelium is vulnerable to noxious substances, resulting in the shedding of cells and decreased protection. Zinc (Zn), an antioxidant and cytoprotectant, can suppress apoptosis in a variety of cells. Here we used the novel Zn-specific fluorophore Zinquin to visualize and quantify labile intracellular Zn in respiratory epithelial cells. Zinquin fluorescence in isolated ciliated tracheobronchial epithelial cells and intact epithelium from sheep and pigs revealed an intense fluorescence in the apical and mitochondria-rich cytoplasm below the cilia. Zinquin fluorescence was quenched by the Zn chelator N,N,N', N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) and increased by the Zn ionophore pyrithione. We also assessed whether changes in intracellular labile Zn would influence susceptibility of these cells to apoptosis by hydrogen peroxide. Our results confirm that Zn deficiency enhanced hydrogen peroxide-induced caspase activation from 1.24 +/- 0.12 to 2.58 +/- 0.53 units. microg protein(-1). h(-1) (P </= 0.05); Zn supplementation suppressed these effects. These findings are consistent with the hypothesis that Zn protects upper respiratory epithelial cells and may have implications for human asthma where there is hypozincemia and epithelial damage.
Authors:
A Q Truong-Tran; R E Ruffin; P D Zalewski
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  279     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2000 Dec 
Date Detail:
Created Date:  2000-12-01     Completed Date:  2000-12-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  L1172-83     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Adelaide, The Queen Elizabeth Hospital, Woodville, South Australia 5011, Australia.
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma, Bronchiolo-Alveolar
Animals
Apoptosis / drug effects,  physiology*
Bronchi / cytology
Butyrates / pharmacology
Caspase 3
Caspases / metabolism
Chelating Agents / pharmacology
Coumarins / pharmacology
Drug Synergism
Enzyme Activation / drug effects
Epithelial Cells / chemistry,  enzymology,  ultrastructure
Ethylenediamines / pharmacology
Fluorescent Dyes
Humans
Hydrogen Peroxide / pharmacology
Lung Neoplasms
Microscopy, Electron
Microscopy, Fluorescence
Oligopeptides / pharmacology
Oxidants / pharmacology
Pulmonary Alveoli / cytology
Quinolones
Respiratory Mucosa / chemistry*,  cytology*
Sheep
Swine
Tosyl Compounds
Trachea / cytology
Tumor Cells, Cultured / chemistry,  cytology,  enzymology
Zinc / analysis*,  physiology*
Chemical
Reg. No./Substance:
0/Butyrates; 0/Chelating Agents; 0/Coumarins; 0/Ethylenediamines; 0/Fluorescent Dyes; 0/Oligopeptides; 0/Oxidants; 0/Quinolones; 0/Tosyl Compounds; 0/benzyloxycarbonyl-aspartyl-glutamyl-valyl-aspartyl-7-amino-4-trifluoromethylcoumarin; 151606-29-0/zinquin; 16858-02-9/N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine; 7440-66-6/Zinc; 7722-84-1/Hydrogen Peroxide; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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