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Lung oxidant changes after zymosan peritonitis: relationship between physiologic and biochemical changes
R Demling1, C Lalonde, Y K Youn
1Longwood Area Trauma Center, Brigham and Women's Hospital, Boston, MA 02115.
The American Review of Respiratory Disease
|November 1, 1992
Summary
Systemic inflammation from zymosan induced severe lung oxidant stress and depleted antioxidants in rats. Lung damage and inflammation persisted for 30 days, even after the initial inflammation resolved.
Area of Science:
- Pulmonary Medicine
- Toxicology
- Inflammation Research
Background:
- Systemic inflammation can impact distant organs.
- Understanding non-bacterial inflammation's effects on the lungs is crucial.
Purpose of the Study:
- To investigate the impact of non-bacteria-dependent systemic inflammation on lung oxidant activity and antioxidant defenses.
- To correlate these changes with physiological and histological alterations in the lungs.
Main Methods:
- Adult male rats were administered intraperitoneal zymosan to induce systemic inflammation.
- Lung tissue was analyzed for oxidant markers (malondialdehyde, oxidized glutathione) and antioxidant levels (reduced glutathione, catalase).
- Physiological (arterial pressure) and histological changes were assessed at multiple time points up to 30 days.
Main Results:
- Zymosan induced significant lung oxidant stress within 24 hours, evidenced by increased malondialdehyde and oxidized glutathione, and depleted reduced glutathione.
- A marked increase in lung neutrophils was observed.
- Arterial oxygen pressure decreased, and lung oxidant markers remained elevated for 30 days, despite resolution of peritonitis.
- Persistent mononuclear cell infiltration and interstitial thickening were noted in lung tissue.
Conclusions:
- Non-bacteria-dependent systemic inflammation causes significant and prolonged lung oxidant stress.
- Lung antioxidant defenses are overwhelmed, and histological damage persists long after the initial inflammatory trigger resolves.
- These findings highlight the sustained impact of systemic inflammation on lung health.