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The role of oxidative processes in emphysema
The American Review of Respiratory Disease
|February 1, 1983
Summary
Cigarette smoke oxidizes lung elastase inhibitors, reducing their activity and potentially causing emphysema. Smoking also impairs elastin repair, contributing to lung damage in smokers.
Area of Science:
- Pulmonary Medicine
- Biochemistry
- Toxicology
Background:
- Pulmonary emphysema is linked to an imbalance between elastase and its inhibitors in the lungs.
- Oxidizing agents, including components of cigarette smoke, can reduce the activity of key elastase inhibitors like alpha 1-proteinase inhibitor (alpha 1-antitrypsin, alpha 1Pi).
Purpose of the Study:
- To investigate the biochemical changes in the lungs induced by cigarette smoking and their correlation with emphysema development.
- To examine the impact of smoking on the activity of lung elastase inhibitors and elastin repair mechanisms.
Main Methods:
- Analysis of alpha 1-proteinase inhibitor (alpha 1-antitrypsin, alpha 1Pi) activity and composition in lung washings from smokers and nonsmokers.
- Assay of hydrolytic activity against a synthetic elastase substrate in lung washes.
- In vitro assessment of cigarette smoke components' effect on elastin cross-link synthesis.
Main Results:
- Alpha 1-proteinase inhibitor (alpha 1-antitrypsin, alpha 1Pi) from smokers' lung washings showed significantly reduced activity and contained oxidized methionine compared to nonsmokers.
- Lung washes from smokers exhibited greater elastolytic activity.
- Acidic components in cigarette smoke inhibited elastin cross-link formation during elastinogenesis in vitro.
Conclusions:
- Cigarette smoking can lead to an acquired imbalance in the lung's elastase/elastase inhibitor system, favoring enzyme activity and contributing to emphysema.
- Smoking interferes with crucial elastin repair processes, further exacerbating lung damage.