Document Detail

Protection against ozone-induced pulmonary inflammation and cell death by endotoxin pretreatment in mice: role of HO-1.
MedLine Citation:
PMID:  11203434     Owner:  NLM     Status:  MEDLINE    
Ozone is a ubiquitous air pollutant that can cause acute pulmonary inflammation and cell injury and may contribute to the exacerbation of chronic pulmonary diseases. The molecular mechanisms of ozone-induced cell injury, as well as protective mechanisms against ozone-injury, are not well understood. Since ozone is a reactive oxidant, and heme oxygenase-1 (HO-1) is an antioxidant enzyme induced by many oxidative stimuli, we hypothesized that HO-1 is one of the protective mechanisms against ozone-induced cell injury, as well as pulmonary inflammation. In the current study, C57Bl/6 mice were pretreated with a low level of endotoxin (lipopolysaccharide, LPS) (0.5 mg/kg) to induce HO-1, and 16 h later were exposed to 1 ppm ozone for 3 h. Endotoxin pretreatment caused a significant protection against ozone-induced pulmonary inflammation and cell injury in bronchoalveolar lavage (BAL) cells. The protection by endotoxin pretreatment against ozone-induced inflammation and necrosis in BAL cells was abolished by the cotreatment with a heme oxygenase inhibitor, tin protoporphyrin IX dichloride (SnPP), suggesting that HO-1 is responsible for the protection against ozone-induced pulmonary inflammation and BAL cell necrosis. Therefore, since HO-1 is induced following ozone exposure, HO-1 may contribute to the development of cellular adaptation to chronic ozone exposure.
L Li; R F Hamilton; A Holian
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Inhalation toxicology     Volume:  12     ISSN:  0895-8378     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2000 Dec 
Date Detail:
Created Date:  2001-01-03     Completed Date:  2001-01-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1225-38     Citation Subset:  IM    
Department of Internal Medicine, Toxicology Program, University of Texas Houston Medical School, Houston, Texas, USA.
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MeSH Terms
Apoptosis / drug effects*
Bronchoalveolar Lavage Fluid / cytology
Cell Survival / drug effects
Heme Oxygenase (Decyclizing) / physiology*
Heme Oxygenase-1
Inflammation / chemically induced*
Lipopolysaccharides / pharmacology*
Lung / drug effects*,  pathology
Membrane Proteins
Mice, Inbred C57BL
Ozone / toxicity*
Grant Support
Reg. No./Substance:
0/Lipopolysaccharides; 0/Membrane Proteins; 10028-15-6/Ozone; EC Oxygenase (Decyclizing); EC Oxygenase-1; EC protein, mouse

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