Protection by N-acetylcysteine against pulmonary endothelial cell damage induced by oxidant injury

R. Sala, E. Moriggi, G. Corvasce, D. Morelli

Research output: Contribution to journalArticle


The protective effect of N-acetylcysteine (NAC) against oxidant lung injury was investigated in a model of acute immunological alveolitis in the rat. Intrapulmonary immune complex deposition into rat lungs, induced by intratracheal infusion of immunoglobulin G (IgG) anti-bovine serum albumin (BSA) antibodies and intravenous injection of the antigen, caused lung damage associated with a marked decrease in [14C]5-hydroxytryptamine ([14C]5HT) uptake capacity, taken as a biochemical marker of endothelial cell function. The oral administration of a single dose of NAC (2 mmol · kg-1) 60 min before antigen/antibody (Ag/Ab) treatment was effective in preventing pulmonary endothelial cell [14C]5HT uptake loss induced by immune complex deposition. The mechanisms involved in this lung protective action of NAC were investigated by studying the antioxidant activity of NAC on hypoxanthine/xanthine oxidase-induced lung damage in vitro, and the effectiveness of the drug as lung glutathione (reduced form) (GSH) precursor in diethylmaleate-depleted rats. The results obtained provide further evidence on the ability of NAC to reduce the susceptibility of lung tissue to free radical-induced damage, by potentiating the antioxidant defence systems.

Original languageEnglish
Pages (from-to)440-446
Number of pages7
JournalEuropean Respiratory Journal
Issue number3
Publication statusPublished - 1993


  • adult respiratory distress syndrome
  • glutathione
  • immune complex alveolitis
  • N-acetylcysteine
  • oxidant lung injury
  • oxygen free radicals

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Fingerprint Dive into the research topics of 'Protection by N-acetylcysteine against pulmonary endothelial cell damage induced by oxidant injury'. Together they form a unique fingerprint.

  • Cite this