Ozone, but not nitrogen dioxide, exposure decreases glutathione peroxidases in epithelial lining fluid of human lung

Citation
Ne. Avissar et al., Ozone, but not nitrogen dioxide, exposure decreases glutathione peroxidases in epithelial lining fluid of human lung, AM J R CRIT, 162(4), 2000, pp. 1342-1347
Citations number
36
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
162
Issue
4
Year of publication
2000
Pages
1342 - 1347
Database
ISI
SICI code
1073-449X(200010)162:4<1342:OBNNDE>2.0.ZU;2-A
Abstract
Antioxidants, such as glutathione peroxidases (GPxs), in epithelial lining fluid (ELF) protect against health effects of oxidant pollutants, which inc ludes O-3 or NO2. We hypothesized that GPxs concentration in ELF is respons ive to O-3 or NO2 exposure. Subjects underwent two 4-h exposures to O-3 (0. 22 ppm) and one to air. In another experiment, subjects underwent 3-h expos ures to air and NO2 (0.6 and 1.5 ppm). Bronchoalveolar lavage (BAL) was per formed immediately or 18 h after O-3 exposure and 3.5 h after each NO2 expo sure. GPx activity and extracellular GPx (eGPx) protein concentrations were determined in ELF, and their relationships to markers of lung function, in flammation, and epithelial permeability were examined. Although the total a mounts were not changed, basal (air) GPx activity (223.6 +/- 24.4 mU/ml), b asal eGPx protein concentration (2.62 +/- 0.25 mu g/ml), and basal ELF dilu tion factor (152.3 +/- 8.4) decreased 40% immediately after O-3 exposure an d remained 30% decreased 18 h after exposure (p = 0.0001). No effect of NO2 exposure on GPxs concentration was detected. There was an inverse correlat ion between baseline ELF eGPx protein concentration and the change in PMN 1 8 h after O-3 exposure (p = 0.04). Thus, O-3 a strong oxidant, decreases bo th GPx activity and eGPx protein in ELF, whereas NO2, a weaker oxidant, doe s not. eGPx in ELF may protect against O-3-induced airway inflammation.