Abstract

The purpose of this study was to clarify what elastase acts primarily to injure the lung tissue when animals are exposed to nitrogen dioxide (NO2). Rats were exposed to 50 ppm NO2 for 5 hours a day on 7 consecutive days. Approximately six animals were sacrificed after the exposure of the 1st, 3rd, 5th and 7th days. On the 1st day, diffuse alveolar edema was seen accompanying deposits of fibrin nets, suggesting the increase of permeability. Inflammatory cell infiltration was seen in terminal bronchioles and alveolar ducts on the 3rd day, however these changes diminished gradually thereafter. The increase of total cell count was seen in bronchoalveolar lavage fluid on day 3 and thereafter. The number of neutrophils was raised markedly on the 3rd day, whereas that of macrophages showed a gradual increase thereafter. The protein concentration of bronchoalveolar lavage fluid increased markedly on the 1st day and was reduced rapidly thereafter. Elastase activity was measured in bronchoalveolar lavage fluid using succinyl-trialanyl-p-nitroanilide as substrate. Total elastase activity was significantly increased on the 1st and 3rd day. Inhibition studies using EDTA and DFP suggested that most of the elastase activity was due to a metaleoprotease. These data suggest that elastase from macrophage may be mainly related to nitrogen dioxide-induced lung injury.

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