Document Detail

Pulmonary inflammation by ambient air particles is mediated by superoxide anion.
MedLine Citation:
PMID:  18236216     Owner:  NLM     Status:  MEDLINE    
Lung inflammation is a key response to increased levels of particulate air pollution (PM); however, the cellular mechanisms leading to this response remain poorly understood. We have previously shown that oxidants are critical mediators of the inflammatory response elicited by inhalation of ambient air particles. Here we tested the possible role of a specific oxidant, superoxide anion, by using the membrane-permeable analog of superoxide dismutase, Mn(III) tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP). Adult Sprague-Dawley rats were instilled with either urban air particles (UAP) or saline. MnTBAP-treated rats received 10 mg/kg (ip) MnTBAP 2 h prior to exposure to UAP. Recruitment of inflammatory cells into bronchoalveolar lavage was evaluated 4 h after instillation. Rats exposed to UAP showed significant increases in the total cell number (8.9 +/- 0.6 x 10(6); sham: 5.1 +/- 0.6 x 10(6), p < .02), the numbers of polymorphonuclear leukocytes (26 +/- 4%; sham: 6 +/- 1%, p < .0001), protein levels (1.2 +/- 0.5 mg/ml, sham: 0.4 +/- 0.1 mg/ml, p < .001), and a trend of increase in myeloperoxidase levels (5 +/- 1; sham: 2 +/- 1 mU/ml) in bronchoalveolar lavage (BAL). Pretreatment with MnTBAP at a dose that prevented UAP-induced increases in oxidants effectively prevented increase in BAL cells (2.7 +/- 0.6 x 10(6), p < .0001 vs. UAP), PMN influx into the lungs (4 +/- 3%, p < .0001 vs. UAP), and increase in myeloperoxidase (2 +/- 1 mU/ml) and protein levels in BAL (0.1 +/- 0.1 mg/ml). These data indicate that superoxide anion is a critical mediator of the inflammatory response elicited by PM deposition in the lung.
Claudia Ramos Rhoden; Elisa Ghelfi; Beatriz González-Flecha
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Inhalation toxicology     Volume:  20     ISSN:  1091-7691     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2008-01-31     Completed Date:  2008-04-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  11-5     Citation Subset:  IM    
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
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MeSH Terms
Free Radicals / adverse effects,  metabolism
Particulate Matter / adverse effects,  metabolism*
Pneumonia / etiology,  metabolism*
Rats, Sprague-Dawley
Superoxides / adverse effects,  metabolism*
Grant Support
Reg. No./Substance:
0/Free Radicals; 0/Particulate Matter; 11062-77-4/Superoxides

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