Document Detail


Biochemical and morphological changes in lung tissue and isolated lung cells of rats induced by short-term nitrogen dioxide exposure.
MedLine Citation:
PMID:  11002389     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To investigate the effects of repeated exposure to nitrogen dioxide (NO2) on antioxidant enzymes in lung tissue and isolated lung cells, rats were continuously exposed to 20 mg/m3 NO2 (10.6 ppm) for 4 days. The activities of glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), and glutathione peroxidase (GSHPx) were measured in the cytosolic fraction of lung tissue of both control and NO2-exposed rats as well as in isolated alveolar macrophages (AMs) and type II cells. Qualitative and quantitative changes in AM and type II cells were studied by electron microscopy and by morphometric analyses using enzyme and immunohistochemistry. NO2 exposure resulted in significantly increased pulmonary activities of G6PDH, GR, and GSHPx, both expressed per lung and per gram of lung weight. Morphometric data show that NO2 exposure significantly increased the number of type II cells, predominantly in the centriacinar region, indicating proliferation of epithelium following cellular injury. Type II cells in lungs of NO2-exposed rats had a squamous, less cuboidal appearance with more lamellar bodies compared to type II cells in lungs of control rats. Compared to control lungs, a higher number of macrophages could be isolated from NO2-exposed lungs, while numbers of type II cells isolated from lungs of control and NO2-exposed rats were the same. Isolated type II cells from control and NO2-exposed rats were polymorphic, with a small number of lamellar bodies and without polarity. Isolated macrophages were rounded and contained many filopodia. NO2 exposure caused increases in the activities of G6PDH and GSHPx in isolated type II cells and of GSHPx in isolated macrophages, when expressed per number of cells. Macrophages and type II cells isolated from control and NO2-exposed rats and re-exposed in vitro to NO2, showed no differences in phagocytosis and viability features. Our results indicate that NO2-induced increases in pulmonary antioxidant enzymes are also reflected in isolated AM and type II cells. Since these lung cells do not display a decreased sensitivities toward an in vitro NO2 exposure, overall increase in antioxidant enzyme activities do not seem to play the most pivotal role in controlling cellular NO2 sensitivity and oxidant defence. Combined data from biochemical, morphological, and morphometric analyses of lungs and lung cells suggest that lung cell and tissue oxidant sensitivity and defence largely depends on the cell and tissue organisation, i.e., cell numbers and morphology as well as the ratio of surface area to cytoplasmic volume.
Authors:
L van Bree; I Rietjens; G M Alink; J Dormans; M Marra; P Rombout
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Human & experimental toxicology     Volume:  19     ISSN:  0960-3271     ISO Abbreviation:  Hum Exp Toxicol     Publication Date:  2000 Jul 
Date Detail:
Created Date:  2000-10-19     Completed Date:  2000-10-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9004560     Medline TA:  Hum Exp Toxicol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  392-401     Citation Subset:  IM    
Affiliation:
Laboratory for Health Effects Research, National Institute of Public Health and Environment, P.O. Box 1, 3720 BA Bilthoven, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism
Cells, Cultured
Cytosol / metabolism
Glutathione Peroxidase / metabolism
Glutathione Reductase / metabolism
Lung / cytology,  metabolism*,  pathology*
Male
Microscopy, Electron
Nitrogen Dioxide / toxicity*
Organ Size / drug effects
Oxidants, Photochemical / toxicity*
Proteins / metabolism
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Oxidants, Photochemical; 0/Proteins; 10102-44-0/Nitrogen Dioxide; EC 1.11.1.9/Glutathione Peroxidase; EC 1.8.1.7/Glutathione Reductase

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