Long-Term Ozone Exposure Attenuates 1-Nitronaphthalene–Induced Cytotoxicity in Nasal Mucosa
Autor: | Charles G. Plopper, Myong Gyong Lee, Bridget C. Boland, Åsa M. Wheelock |
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Rok vydání: | 2008 |
Předmět: |
Male
Pulmonary and Respiratory Medicine Pathology medicine.medical_specialty Ozone medicine.medical_treatment Clinical Biochemistry Intraperitoneal injection Mucous membrane of nose Naphthalenes Pharmacology Models Biological Rats Sprague-Dawley chemistry.chemical_compound Olfactory Mucosa medicine Animals Toxicity Tests Chronic Molecular Biology Air Pollutants Goblet cell Dose-Response Relationship Drug Histocytochemistry Articles Cell Biology Hydrogen-Ion Concentration Periodic Acid-Schiff Reaction Transitional epithelium Rats Nasal Mucosa medicine.anatomical_structure chemistry Toxicity Respiratory epithelium Alcian Blue Injections Intraperitoneal Toxicant |
Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 38:300-309 |
ISSN: | 1535-4989 1044-1549 |
DOI: | 10.1165/rcmb.2005-0416oc |
Popis: | 1-Nitronaphthalene (1-NN) and ozone are cytotoxic air pollutants commonly found as components of photochemical smog. The mechanism of toxicity for 1-NN involves bioactivation by cytochrome P450s and subsequent adduction to proteins. Previous studies have shown that 1-NN toxicity in the lung is considerably higher in rats after long-term exposure to ozone compared with the corresponding filtered air–exposed control rats. The aim of the present study was to establish whether long-term exposure to ozone alters the susceptibility of nasal mucosa to the bioactivated toxicant, 1-NN. Adult male Sprague-Dawley rats were exposed to filtered air or 0.8 ppm ozone for 8 hours per day for 90 days, followed by a single treatment with 0, 12.5, or 50.0 mg/kg 1-NN by intraperitoneal injection. The results of the histopathologic analyses show that the nasal mucosa of rats is a target of systemic 1-NN, and that long-term ozone exposure markedly lessens the severity of injury, as well as the protein adduct formation by reactive 1-NN metabolites. The antagonistic effects were primarily seen in the nasal transitional epithelium, which corresponds to the main site of histologic changes attributed to ozone exposure (goblet cell metaplasia and hyperplasia). Long-term ozone exposure did not appear to alter susceptibility to 1-NN injury in other nasal regions. This study shows that long-term ozone exposure has a protective effect on the susceptibility of nasal transitional epithelium to subsequent 1-NN, a result that clearly contrasts with the synergistic toxicological effect observed in pulmonary airway epithelium in response to the same exposure regimen. |
Databáze: | OpenAIRE |
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