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

R Sala, E Moriggi, G Corvasce, D Morelli
European Respiratory Journal 1993 6: 440-446; DOI:
R Sala
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E Moriggi
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G Corvasce
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D Morelli
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Abstract

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.

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Protection by N-acetylcysteine against pulmonary endothelial cell damage induced by oxidant injury
R Sala, E Moriggi, G Corvasce, D Morelli
European Respiratory Journal Mar 1993, 6 (3) 440-446;

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Protection by N-acetylcysteine against pulmonary endothelial cell damage induced by oxidant injury
R Sala, E Moriggi, G Corvasce, D Morelli
European Respiratory Journal Mar 1993, 6 (3) 440-446;
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