Effect of 0.25 ppm Ozone exposure on pulmonary damage induced by bleomycin

Manuel Oyarzún,Sergio González,Nelson Dussaubat

doi:10.4067/s0716-97602005000400007

Manuel Oyarzún, Sergio González + Show 1 more

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https://doi.org/10.4067/s0716-97602005000400007

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Abstract

To study the effect of ozone in a chronically damaged lung, we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O3 in rats with bleomycin-induced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (1 U/100 g body weight) and, 30 days later, exposed to 0.25 ppm 03 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O3 exposure. BLM-induced lung damage did not change after 60 days of intermittent O3 exposure. Five days of O3 exposure increased the mean score of BLM-induced pulmonary inflammation and fibrosis (p=0.06). Frequency of bronchopneumonia increased from 1/7 to 6/6 (p <0.001), suggesting that a short-term exposure to O3 in a previously damaged lung might be a risk factor for developing further lung injury.

Highlights

Because individuals with chronic lung disease are a high-risk group for the effects of air pollutants (Bascom, 1996; Oyarzún et al, 1998), experimental animal models of pulmonary emphysema (Yokoyama et al, 1987) and airway inflammation (Last et al, 2004) have been used to study the effects of ozone (O3)
Instilled BLM produces lung inflammation within 24 hours followed by a patchy pulmonary fibrosis 14 days after exposure
In the series of rats treated with BLM + O3, emphysema was absent, focal lung interstitial fibrosis was mild, and the inflammatory reaction was mild to moderate, they were not significant different as compared to the scores of rats treated with BLM + air (p=0.06; MannWhitney’s test, Table I and Fig 1b)

Summary

Introduction

Because individuals with chronic lung disease are a high-risk group for the effects of air pollutants (Bascom, 1996; Oyarzún et al, 1998), experimental animal models of pulmonary emphysema (Yokoyama et al, 1987) and airway inflammation (Last et al, 2004) have been used to study the effects of ozone (O3). Another suitable model may be bleomycin-induced pulmonary fibrosis (FBLM) in rats (Dussaubat et al, 1995, Cooper 2000, Borzone et al, 2001). The interaction of O2 species with essential biomolecules can lead to changes in their structure and function, if these prooxidants are not adequately balanced by a similar rate of cellular antioxidants, which constitutes the molecular basis of oxidative stress phenomenon (Fernández et al, 1996)

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