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Comparative sensitivity of measurements of lung damage made by bronchoalveolar lavage after short-term exposure of rats to ozone
Authors:D J Guth  D L Warren  J A Last
Abstract:Consequences of exposure of rats for 2 days or less to O3 at various concentrations between 0.12 and 0.96 ppm were measured using several assays performed on bronchoalveolar lavage fluid. Changes in apparent lung permeability were assessed by measurement of recovery of labelled bovine serum albumin in lung lavage fluid after intravenous injection ("permeability index"). The relative sensitivity of this assay was compared with the sensitivity of measurements of changes in protein and of enzyme content in lavage fluid. Permeability index increased in an exposure concentration-dependent manner after 6 or 24 h of exposure to O3 at or above levels of 0.4 ppm. Permeability index was also increased after 2 days of exposure to 0.2 ppm of O3. The activities of lactate dehydrogenase, acid phosphatase, and N-acetyl-beta-D-glucosaminidase in lung lavage fluid were less sensitive indicators of O3 damage than was altered permeability index. Increased lactate dehydrogenase activity could only be detected after continuous exposure of rats for at least 1 day to 0.64 (or higher) ppm of O3, while acid phosphatase and N-acetyl-beta-D-glucosaminidase activities were increased after exposure of rats to O3 at 0.4 ppm or above for 1 day. Activities of these enzymes were not increased after 6 h of exposure to 0.64 ppm of O3 or after 2 days of exposure to 0.2 ppm. Increased lavage protein content was the most sensitive measurement of the consequences of O3 exposure to rats in these protocols. The lavagable protein content increased after exposure of rats to O3 for 6 h at 0.4 ppm and for 1 or 2 days of exposure to 0.12 ppm, the current peak hourly National Ambient Air Quality standard for O3. While the biological significance of these observations remains to be determined, measurement of lavage protein content is a simple, sensitive indicator of acute changes in the lung caused by exposure to environmentally relevant concentrations of O3.
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