ACUTE AND PROGRESSIVE LUNG INJURY AFTER CONTACT WITH PHORBOL-MYRISTATE ACETATE
- 1 January 1982
- journal article
- research article
- Vol. 107 (1) , 29-35
Abstract
Because of its potent ability to activate leukocytes and macrophages, resulting in the generation of large amounts of O2 products (O2-, H2O2), phorbol myristate acetate (PMA) was instilled into the airways of rats. The resulting acute lung injury was dose-dependent on the amount of PMA employed, was chiefly confined anatomically to the alveolar and interstitial compartments, was neutrophil-independent, and was inhibited by catalase but not by superoxide dismutase. The generation of H2O2 was a major mechanism involved in this model of acute lung injury. A progressive pattern of lung injury developed after exposure to PMA, with the onset of an interstitial fibrotic reaction by the 6th day. Acute and progressive injury occurred in lungs of rats when H2O2.This publication has 12 references indexed in Scilit:
- Role of oxygen metabolites in immune complex injury of lung.The Journal of Immunology, 1981
- In vivo damage of rat lungs by oxygen metabolites.Journal of Clinical Investigation, 1981
- SUPPRESSION BY SUPEROXIDE-DISMUTASE OF IMMUNE-COMPLEX-INDUCED PULMONARY ALVEOLITIS AND DERMAL INFLAMMATION1981
- Copper chelator enhancement of bleomycin cytotoxicityCancer, 1980
- Rat alveolar macrophages require NADPH for superoxide production in the respiratory burst. Effect of NADPH depletion by paraquat.Journal of Biological Chemistry, 1980
- Liver Necrosis and Lipid Peroxidation in the Rat as the Result of Paraquat and Diquat AdministrationJournal of Clinical Investigation, 1980
- Oxidative mechanisms of monocyte-mediated cytotoxicity.Proceedings of the National Academy of Sciences, 1980
- Generation of chemiluminescence by a particulate fraction isolated from human neutrophils. Analysis of molecular events.Journal of Clinical Investigation, 1979
- Acute Immunologic Pulmonary AlveolitisJournal of Clinical Investigation, 1974