RT Journal Article
SR Electronic
T1 Protection by N-acetylcysteine against pulmonary endothelial cell damage induced by oxidant injury
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 440
OP 446
DO 10.1183/09031936.93.06030440
VO 6
IS 3
A1 R Sala
A1 E Moriggi
A1 G Corvasce
A1 D Morelli
YR 1993
UL http://erj.ersjournals.com/content/6/3/440.abstract
AB 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.