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Background  Exposure to chlorine (Cl 2 ) causes airway injury, characterized by oxidative damage, an influx of inflammatory cells and airway hyperresponsiveness. We hypothesized that Cl 2 -induced airway injury may be attenuated by antioxidant treatment, even after the initial injury.    Methods  Balb/C mice were exposed to Cl 2  gas (100 ppm) for 5 mins, an exposure that was established to alter airway function with minimal histological disruption of the epithelium. Twenty-four hours after exposure to Cl 2 , airway responsiveness to aerosolized methacholine (MCh) was measured. Bronchoalveolar lavage (BAL) was performed to determine inflammatory cell profiles, total protein, and glutathione levels. Dimethylthiourea (DMTU;100 mg/kg) was administered one hour before or one hour following Cl 2  exposure.    Results  Mice exposed to Cl 2  had airway hyperresponsiveness to MCh compared to control animals pre-treated and post-treated with DMTU. Total cell counts in BAL fluid were elevated by Cl 2  exposure and were not affected by DMTU treatment. However, DMTU-treated mice had lower protein levels in the BAL than the Cl 2 -only treated animals. 4-Hydroxynonenal analysis showed that DMTU given pre- or post-Cl 2  prevented lipid peroxidation in the lung. Following Cl 2  exposure glutathione (GSH) was elevated immediately following exposure both in BAL cells and in fluid and this change was prevented by DMTU. GSSG was depleted in Cl 2  exposed mice at later time points. However, the GSH/GSSG ratio remained high in chlorine exposed mice, an effect attenuated by DMTU.    Conclusion  Our data show that the anti-oxidant DMTU is effective in attenuating Cl 2  induced increase in airway responsiveness, inflammation and biomarkers of oxidative stress.

Dimethylthiourea protects against chlorine induced changes in airway function in a murine model of irritant induced asthma