Document Detail

Lung oxidative response after acute coal dust exposure.
MedLine Citation:
PMID:  15364596     Owner:  NLM     Status:  MEDLINE    
Coal dust exposure can induce an acute alveolar and interstitial inflammation that can lead to chronic pulmonary diseases. The objective of this study was to describe the acute and later effects of acute coal dust exposure in lung parenchyma and the involvement of reactive oxygen species in coal dust effects. Forty-eight male Wistar rats (200-250 mg) were separated into four groups: 48 h, 7 days, 30 days, and 60 days after coal dust instillation. Gross mineral coal dust (3 mg/0.5 mL saline) was administered directly in the lungs of the treatment group by intratracheal instillation. Control animals received only saline solution (0.5 mL). Lipid peroxidation was determined by the quantity of thiobarbituric acid-reactive species (TBARS), oxidative damage to protein was obtained by the determination of carbonyl groups, the total radical-trapping antioxidant parameter (TRAP) was estimated by luminol chemoluminescence emission, catalase activity was measured by the rate of decrease in hydrogen peroxide, and superoxide dismutase activity was assayed by the inhibition of adrenaline autooxidation. Histological evaluation of coal dust-treated rats demonstrated an inflammatory infiltration after 48 h of the exposure. Initially, this was a cellular infiltration suggestive of lymphocyte infiltration with lymphoid hyperplasia that remained until 7 days after induction. This initial response was followed by a chronic inflammatory infiltration characterized by aggregates of macrophages 30 days after induction. This inflammatory response tended to resolve 60 days after induction, being similar to that of control animals. During both the acute and chronic phases of lung inflammation we observed a decrease in the TRAP in the lung of coal dust-exposed animals compared to that in control animals. We also observed an activation of superoxide dismutase 60 days after coal dust exposition. TBARS were increased 60 days after coal dust exposure and protein carbonyl groups increased at all times after coal dust exposure (48 h, 7 days, 30 days, and 60 days). These data suggested a biphasic inflammatory response and the involvement of oxidative damage in coal dust-induced lung damage.
Ricardo A Pinho; Fernanda Bonatto; Michael Andrades; Mário Luis C Frota; Cristiane Ritter; Fábio Klamt; Felipe Dal-Pizzol; Jane M Uldrich-Kulczynski; José Cláudio F Moreira
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Environmental research     Volume:  96     ISSN:  0013-9351     ISO Abbreviation:  Environ. Res.     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-09-14     Completed Date:  2004-10-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147621     Medline TA:  Environ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  290-7     Citation Subset:  IM    
Laboratório de Estresse Oxidativo/Departamento de Bioquímica/UFRGS, Ramiro Barcelos, 2600 (anexo), 90620-050 Porto Alegre, Brazil.
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MeSH Terms
Free Radicals*
Inhalation Exposure*
Lung / pathology*
Oxidative Stress*
Rats, Wistar
Thiobarbituric Acid Reactive Substances / analysis
Reg. No./Substance:
0/Coal; 0/Dust; 0/Free Radicals; 0/Thiobarbituric Acid Reactive Substances

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