Oxidative stress in chlorine exposed A/J mice.
Authors
Martin-JG; Campbell-HR; Iijima-H; Maghni-K; Malo-JL; Gautrin-D; Eidelman-DH
Source
Am J Respir Crit Care Med 2001 Apr; 163(5)(2)(Suppl):A810
Abstract
Acute chlorine (CI2) exposure is a cause of occupational asthma. CI2 has been shown to evoke a neutrophilic inflammation and airway remodeling in the rat. Neutrophils are capable of producing several reactive oxygen and nitrogen species. Of particular interest is NO2 that reacts with HOCI to form 3-nitrotyrosine (3NT) and 3-chlorotyrosine, markers of inflammation-mediated protein modification and tissue injury. In this study, we examined effects of Cl2 exposure on oxidative and nitrosative stress in A/J mice. Mice (25g) were exposed to 0, 100 or 800 ppm CI2 for 5 min and monitored for 24 h. Animals were then sacrificed and bronchoalveolar lavage (BAL), immuno-histochemistry and Western analysis were performed. In the 800 ppm group, there was epithelial desquamation and immuno-histochemical staining showed neutrophils that were strongly positive for 3NT and inducible nitric oxide synthase (iNOS). At 100 ppm, there was less epithelial damage and cells stained positively for iNOS. Western blotting and densitometry showed that iNOS expression was increased by 205% at 100 ppm, 85% at 800 ppm when compared to 0 ppm. In lung tissue, oxidation of component proteins rich in carbonyl groups was examined by Western blotting for DNPH (2,4-dinitrophenylhydrazone-hydrazone). Levels of oxidized proteins of molecular weights 51, 57, 62, and 70 kDa increased in a dose-dependent manner with CI2 concentration. These findings suggest that CI2 exposure causes oxidative and nitrosative stress in association with leading to airway epithelial damage.
Keywords
Lung-function; Lung-disease; Breathing; Inhalants; Chlorine-compounds; Respiratory-system-disorders; Pulmonary-system-disorders; Cellular-function; Lung-function; Animal-studies; In-vivo-study; Laboratory-animals; Oxidative-processes
Identifying No.
Grant-Number-R01-OH-004058
Priority Area
Disease and Injury: Asthma and Chronic Obstructive Pulmonary Disease
Source Name
American Journal of Respiratory and Critical Care Medicine. Abstracts of the American Thoracic Society 2001 International Conference, May 18-23, 2001, San Francisco, California
Performing Organization
Hospital du Sacre-Coeur, Montreal, Quebec
