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Am J Physiol Lung Cell Mol Physiol 285: L1037-L1045, 2003. First published August 15, 2003; doi:10.1152/ajplung.00008.2003
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Protein nitration in rat lungs during hyperoxia exposure: a possible role of myeloperoxidase

Telugu A. Narasaraju, Nili Jin, Chintagari R. Narendranath, Zhongming Chen, Deming Gou, and Lin Liu

Department of Physiological Sciences, Oklahoma State University, Stillwater, Oklahoma 74078

Submitted 9 January 2003 ; accepted in final form 28 July 2003

Several studies have suggested that exposure to hyperoxia causes lung injury through increased generation of reactive oxygen and nitrogen species. The present study was aimed to investigate the effects of hyperoxia exposure on protein nitration in lungs. Rats were exposed to hyperoxia (>95%) for 48, 60, and 72 h. Histopathological analysis showed a dramatic change in the severity of lung injury in terms of edema and hemorrhage between 48- and 60-h exposure times. Western blot for nitrotyrosine showed that several proteins with molecular masses of 29-66 kDa were nitrated in hyperoxic lung tissues. Immunohistochemical analyses indicate nitrotyrosine staining of alveolar epithelial and interstitial regions. Furthermore, immunoprecipitation followed by Western blot revealed the nitration of surfactant protein A and t1{alpha}, proteins specific for alveolar epithelial type II and type I cells, respectively. The increased myeloperoxidase (MPO) activity and total nitrite levels in bronchoalveolar lavage and lung tissue homogenates were observed in hyperoxic lungs. Neutrophils and macrophages isolated from the hyperoxia-exposed rats, when cocultured with a rat lung epithelial L2 cell line, caused a significant protein nitration in L2 cells. Inclusion of nitrite further increased the protein nitration. These studies suggest that protein nitration during hyperoxia may be mediated in part by MPO generated from activated phagocytic cells, and such protein modifications may contribute to hyperoxia-mediated lung injury.

lung injury; coculture


Address for reprint requests and other correspondence: L. Liu, Dept. of Physiological Sciences, Oklahoma State Univ., 264 McElroy Hall, Stillwater, OK 74078 (E-mail: liulin{at}okstate.edu).




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