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Journal of Endotoxin Research, Vol. 1, No. 2, 108-113 (1994)
DOI: 10.1177/096805199400100205
© 1994 SAGE Publications

Protection against oxygen toxicity by lipid A: role of Mn superoxide dismutase

J.T. Berg

Research Service, Samuel S. Stratton Department of Veterans Affairs Medical Center, Departments of Physiology and Cell Biology, Medicine and Anesthesiology, Albany Medical College, Albany, NY, USA

G. Tang

Research Service, Samuel S. Stratton Department of Veterans Affairs Medical Center, Departments of Physiology and Cell Biology, Medicine and Anesthesiology, Albany Medical College, Albany, NY, USA

M.F. Tsan

Research Service, Samuel S. Stratton Department of Veterans Affairs Medical Center, Departments of Physiology and Cell Biology, Medicine and Anesthesiology, Albany Medical College, Albany, NY, USA

Previous studies have shown that diphosphoryl lipid A (DPL), but not monophosphoryl lipid A (MPL), protects rats against lethal hyperoxia. However, the mechanism of DPL-induced 02 resistance is not clear. In this study, we demonstrated that tracheal insufflation of 5 µg endotoxin (LPS) or DPL, but not MPL, markedly prolonged the survival of rats exposed to 100% O2. LPS was more protective than DPL, while DPL induced more alveolar inflammatory response and tumor necrosis factor (TNF) release. Both LPS and DPL caused a selective enhancement of pulmonary Mn superoxide dismutase (SOD) mRNA without affecting levels of CuZnSOD and catalase mRNAs. In contrast, MPL caused some release of TNF into the alveolar space, but did not produce an inflammatory response and had no effect on pulmonary MnSOD mRNA. These results support a potential role for pulmonary MnSOD in LPS- and DPL-induced 02 tolerance.


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