Vitamin C inhibits the diisocyanate-induced lung inflammatory response in mice

Abstract

Background: Vitamin C (vit C) is an antioxidant involved in scavenging free radicals generated during cellular metabolism. It has been found that isocyanate-induced lung disease is an oxidant stress-dependent pulmonary inflammation. The goal of this study was to evaluate the antioxidant effect of vit C on the course of allergic inflammation in the lungs in an experimental murine model of toluene diisocyanate (TDI-)induced asthma. Methods: BALB/cJ/Han/IMP mice were divided into six different groups: Group I: unsensitized control; Group II: TDI control; Group III -VI:TDI + vitamin C in four different doses. All mice were exposed first intranasally and then in an inhalation chamber to TDI in the air. After the final exposure, bronchoalveolar lavage fluid (BALF) was collected and changes induced in levels of inflammatory cells, and some key cytokines (IL-4, TNFa, IFNg) were evaluated. In addition, thiobarbituric acid reactive substance (TBARS) levels in plasma and liver homogenates were evaluated. Results: Total number of cells in the BALF of vit C-treated mice were lower than in the BALF of the TDI controls. A significant decrease in BALF neutrophil levels and IL-4, TNFa, IFNg levels were decreased in the BALF of most of vit C-treated mice compared to TDI controls. TBARS levels were decreased in the serum of vit C-supplemented mice as compared to TDI control. There was an increase in TBARS levels in the livers of mice that received the highest dose of the vitamin. Conclusion: The results of this experiment suggest that vitamin C may reduce inflammation and oxidative stress in the lungs of TDI-treated mice.