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Nitric oxide-induced prostaglandin release by rat alveolar macrophages.
Toxicologist 1997 Mar; 36(1)(Part 2):77
There is a growing body of evidence demonstrating links between the mtnc oxide synthase and cyclooxygenase pathways. We hypothesized that nitric oxide (NO) might increase the release of prostaglandins (PG) by alveolar macrophages (AM). AM were obtained from male Sprague-Dawley rats by bronchoalveolar lavage and were cultured for 6 hours:!: spermine-NO, a NO-liberating compound. Some cultures also contained superoxide dismutase (SOD). At the end of the culture period, cell supernatants were collected and assayed for NO products (Greiss method) and PGE2 (enzyme-linked immunoassay). The spermine-NO complex increased NO products in the culture medium by 19-fold (22.5 vs. 424 J-lM). Such elevated NO levels increased PGE2 release from AM 7-fold (73.3 vs. 545 pg/ml). SOD increased NO products in some cultures and had no effect in other cultures; in all cultures SOD increased PGE2 release an average of 4-fold (73.3 vs 314 pg/ rol). The combination of spermine-NO and SOD elevated PGE2 (770 pg/ml). This effect of SOD on NO-induced PGE2 release appeared to be additive, not synergistic. These results demonstrate that NO increases the release of PGE2 from AM. Induction of NO production has been associated with in vivo exposure to various particulates. Since PG have been shown to decrease fibroblast proliferation, NO-enhanced PGE2 release could represent a controlling or counterbalancing mechanism which may limit particle-induced fibrogenesis.
Toxic-dose; Toxic-materials; Toxins; Exposure-assessment; Exposure-levels; Exposure-limits; Alveolar-cells; Lung-tissue; Lung-disorders; Lung-cells; Respiratory-system-disorders; Pulmonary-system-disorders; Laboratory-animals; Animal-studies; Animals
Issue of Publication
The Toxicologist. Society of Toxicology 36th Annual Meeting, March 9-13, 2006, Cincinnati, Ohio
Page last reviewed: May 5, 2020
Content source: National Institute for Occupational Safety and Health Education and Information Division