Abstract
Cigarette smoking is well established as the cause of the majority of cases of emphysema. However, the mechanisms by which exposure of the lung to smoke causes the destruction of the lung parenchyma are not known. Oxidation probably contributes to the progression of this disease in several different ways. Oxidants present in the smoke itself or those generated by inflammatory cells in response to the particulate phase of the smoke inactivate proteinase inhibitors, and the increased inflammatory cells produce and release additional proteinases. The expression and activity of metalloproteinases, which have recently been implicated in the pathogenesis of emphysema, are regulated by redox status. Finally, oxidative damage to structural proteins may potentiate their degradation by the increased proteolytic burden.

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