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Toxicological Sciences 54, 452-461 (2000)
Copyright © 2000 by the Society of Toxicology

Quantitation and Localization of Pulmonary Manganese Superoxide Dismutase and Tumor Necrosis Factor {alpha} following Exposure to Ozone and Nitrogen Dioxide

Barbara L. Weller1, Hanspeter Witschi and Kent E. Pinkerton

Center for Comparative Respiratory Biology and Medicine, California Regional Primate Research Center, Institute of Toxicology and Environmental Health, University of California, One Shields Avenue, Davis, California 95616

Tumor necrosis factor {alpha} (TNF{alpha}) and manganese superoxide dismutase (MnSOD) are thought to play critical roles in the process of lung injury, repair, and disease. The induction of TNF{alpha} and MnSOD were examined in a model of progressive pulmonary fibrosis along the length of the alveolar duct in rats exposed for 1, 5, and 8 weeks to a combination of 0.8 ppm ozone and 14.4 ppm nitrogen dioxide. This oxidant injury model results in a triphasic response with an initial inflammatory stage during weeks 1–3, followed by a partial resolution at weeks 4–5, and a final stage of rapidly progressive fibrosis during weeks 6–8. Changes in TNF{alpha} and MnSOD labeling for the proximal and distal alveolar ducts of the lungs were quantified using immunohistochemistry and morphometric techniques at 1, 5, and 8 weeks of exposure. A significant elevation in MnSOD was noted in alveolar macrophages and interstitial cells of the proximal and distal portions of the alveolar duct following 8 weeks of exposure. Labeling for TNF{alpha} only in the proximal region of the alveolar duct, was significantly increased in alveolar macrophages after 1 and 8 weeks of exposure, while a significant increase in TNF{alpha} labeling of interstitial cells in proximal regions was noted at all time points. We conclude that MnSOD is elevated in areas of focal injury as well as the more distal protected areas of the lungs, while TNF{alpha} correlates strongly with both the temporal and spatial aspects of greatest cellular injury in the lungs.

Key Words: lung; fibrosis; cytokine; antioxidant; tumor necrosis factor {alpha} (TNF{alpha}); manganese superoxide dismutase (MnSOD).


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