BACKGROUND/AIMS: Lung involvement due to inflammatory bowel disease (IBD) is frequent, however the pathogenic mechanism is still debatable. Although the evidence of inflammation in colonic and lung tissue has been documented, the possible effect of oxidative stress in lung tissue has not been evaluated to date. We sought to assess the effects of oxidant/antioxidants on lung tissue in a model of experimental colitis. METHODOLOGY: Colitis was induced with intra-colonic administration of 4% acetic acid. Control group received isotonic saline. Serum and lung tissue markers of oxidative stress were explored. RESULTS: Serum total oxidant status was significantly higher in the colitis group than the controls while total antioxidant status was similar. The determinants of oxidants including lipid peroxidation assay and myeloperoxidase activity were significantly higher in the lung tissue of the colitis group whereas the indicators of antioxidant capacity determined as superoxide dismutase, catalase, glutathione and glutathione peroxidase were decreased (p<0.05). CONCLUSIONS: This study showed that oxidative stress is not restricted to the bowel and the lung is a main target of oxidant overload. Pulmonary injury caused by increased oxidant stress may be the underlying reason of pulmonary involvement due to IBD.
BACKGROUND/AIMS: Lung involvement due to inflammatory bowel disease (IBD) is frequent, however the pathogenic mechanism is still debatable. Although the evidence of inflammation in colonic and lung tissue has been documented, the possible effect of oxidative stress in lung tissue has not been evaluated to date. We sought to assess the effects of oxidant/antioxidants on lung tissue in a model of experimental colitis. METHODOLOGY:Colitis was induced with intra-colonic administration of 4% acetic acid. Control group received isotonic saline. Serum and lung tissue markers of oxidative stress were explored. RESULTS: Serum total oxidant status was significantly higher in the colitis group than the controls while total antioxidant status was similar. The determinants of oxidants including lipid peroxidation assay and myeloperoxidase activity were significantly higher in the lung tissue of the colitis group whereas the indicators of antioxidant capacity determined as superoxide dismutase, catalase, glutathione and glutathione peroxidase were decreased (p<0.05). CONCLUSIONS: This study showed that oxidative stress is not restricted to the bowel and the lung is a main target of oxidant overload. Pulmonary injury caused by increased oxidant stress may be the underlying reason of pulmonary involvement due to IBD.