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Published ahead of print on February 12, 2004, doi:10.1165/rcmb.2003-0377OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 1, July 2004, 43-53

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Submitted on October 22, 2003
Revised on February 12, 2004

High Levels of Catalase and GPx Activity Dampen H2O2 Signaling in Human Alveolar Macrophages

A. Brent Carter1*, Linda A Tephly1, Sujatha Venkataraman2, Larry W Oberley2, Yuping Zhang2, Garry R Buettner2, Douglas R Spitz2, and Gary W Hunninghake1

1 Internal Medicine, University of Iowa, Iowa City, IA, USA, 2 Radiation Oncology, University of Iowa, Iowa City, IA, USA

* To whom correspondence should be addressed. E-mail: brent-carter{at}uiowa.edu.

Results are presented that support the hypothesis that adequate steady-state levels of hydrogen peroxide (H2O2) are required to overcome the effects of high catalase and glutathione peroxidase (GPx) expression for p38 MAP kinase activation and TNF-{alpha} gene expression in human alveolar macrophages stimulated with asbestos. We found significant differences in the types and amounts of reactive oxygen species (ROS) generated in human blood monocytes compared to human alveolar macrophages. This difference in ROS production is related, in part, to the differences in antioxidant enzyme expression and activity. Most importantly, catalase and glutathione peroxidase (GPx) activities were significantly increased in alveolar macrophages compared to blood monocytes. Asbestos activated the p38 MAP kinase and induced TNF-{alpha} gene expression only in blood monocytes. Increasing the steady-state levels of H2O2 by utilizing polyethylene glycol superoxide dismutase (PEG-SOD), an antioxidant that crosses the cell membrane, or aminotriazole, an irreversible inhibitor of catalase, allowed the p38 MAP kinase to be activated in alveolar macrophages. In addition, asbestos-stimulated macrophages cultured with PEG-SOD had a significant increase in gene expression mediated by the TNF-{alpha} promoter. These results demonstrate that high catalase and GPx activity in human alveolar macrophages limits the effectiveness of H2O2 to act as a mediator of inflammatory gene expression.




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