• 1 May 1989
    • journal article
    • research article
    • Vol. 27  (5) , 238-241
Abstract
Cigarette smoke reduces the elastase inhibitory capacity (EIC) of .alpha.1-antitrypsin by an oxidative process and thus may promote the pathogenetic bases for the development of pulmonary emphysema. The present study was performed with the aim to evaluate the protective activity of erdosteine, a novel thiol derivative endowed with reducing properties, against the functional inactivation of .alpha.1-AT induced by smoke. For the purpose, a double-blind study was carried out on 24 healthy smokers divided into two groups orally treated with placebo or erdosterine 900 mg/day for one month. The antigenic and functional .alpha.1-AT was measured in bronchoalveolar (BAL) fluids and sera before and shortly after the last treatment. The findings indicate that the loss of EIC of .alpha.1-AT in BAL fluids can be partially prevented by pharmacological treatment. In this regard, it is reasonable to hypothesize that the reestablishment of the oxidant-antioxidant balance in favor of the antioxidants would be useful as a therapeutic strategy to arrest or at least delay the emphysematous process.