Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide

Abstract

Short-term exposure to cigarette smoke (CS) or lipopolysaccharide (LPS) leads to acute lung inflammation through oxidant–antioxidant imbalance. We studied the response in mice exposed to smoke or LPS during five consecutive days, as measured by superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, as well as lipid peroxidation and nitric oxide levels in bronchoalveolar lavage fluid (BALF), lung homogenates, and plasma. Control mice were exposed to ambient air. Exposure to CS or LPS led to a similar influx of alveolar macrophages and neutrophils into the BALF; however, hydroxyproline levels were increased only in the CS group ( p<0.001); SOD activity was increased in the BALF ( p<0.001) and lung homogenates ( p<0.05) of the CS group but was decreased in the BALF ( p<0.05), lung homogenates ( p<0.05) and plasma ( p<0.01) of the LPS group. CAT activity was increased in the BALF ( p<0.01), lung homogenates ( p<0.001) and plasma ( p<0.05) of the CS group but decreased in the BALF ( p<0.001) and plasma ( p<0.05) of the LPS group. GPx activity was reduced in the BALF ( p<0.01) and plasma ( p<0.01) of both the CS and LPS groups. Lipid peroxidation was increased in the BALF ( p<0.001) and lung homogenates ( p<0.001) of the CS group. Finally, the levels of nitrite were reduced in the CS ( p<0.01) and LPS ( p<0.001) groups. Our data show that the activity profiles of enzymes contributing to oxidant–antioxidant imbalance in the lungs differ depending on the inflammatory stimulus, and that SOD, CAT and GPx may be useful markers of oxidative stress in acute lung inflammation induced by exposure to CS.