Endotoxin increases superoxide dismutase in cultured bovine pulmonary endothelial cells.
Manganous (Mn) and copper zinc (CuZn) superoxide dismutase (SOD) concentrations and glutathione peroxidase (GSH-Px) and catalase (CAT) activities were measured in cultured bovine pulmonary endothelial cells with and without exposure to Escherichia coli endotoxin (10(-1) micrograms/ml) over intervals of 0.5-24 h. The activities of two mitochondrial marker enzymes, fumarase and cytochrome-c oxidase, were also measured. Endotoxin exposure caused a marked increase (9-fold) in endothelial cell Mn SOD content without significant effects on GSH-Px, CAT, fumarase, or cytochrome-c oxidase activities. Endotoxin induced a slight decrease in CuZn SOD content over 24 h. This is the first report of a selective effect of endotoxin on Mn SOD in pulmonary endothelial cells. The response appears to be independent of an increase in mitochondrial activity (no change was observed in cytochrome-c oxidase or fumarase activities). These findings support the notion that endotoxin increases generation of toxic oxygen metabolites within pulmonary endothelial cells. An endotoxin-induced increase in Mn SOD could contribute to the reported protective effect of endotoxin against oxygen toxicity in these cells.
D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D003576:Electron Transport Complex IV / Q000378:metabolism; D004727:Endothelium / Q000201:enzymology; D004731:Endotoxins / Q000494:pharmacology*; D005649:Fumarate Hydratase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008168:Lung / Q000201:enzymology*; D008928:Mitochondria / Q000201:enzymology; D013482:Superoxide Dismutase / Q000378:metabolism*
D001427:Bacterial Toxins; D004731:Endotoxins; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003576:Electron Transport Complex IV; D005649:Fumarate Hydratase