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1 Dept of Internal Medicine, Division for Pulmonary Diseases, and 2 Institute for Surgical Research, Klinikum Grosshadern, Ludwig-Maximilians-University of Munich, Munich, Germany
CORRESPONDENCE: J. Behr, Department of Internal Medicine I, Division for Pulmonary Diseases, Klinikum Grosshadern, University of Munich, Marchioninistr. 15, 81377, Munich, Germany. Fax: 49 8970958877. E-mail: jbehr@med1.med.uni-muenchen.de
Keywords: fibrosing alveolitis, glutathione, interleukin-8, myeloperoxidase, oxidative activity
Received: January 15, 2001
Accepted November 2, 2001
J. Behr was supported by Wilhelm Sander-Stiftung
Extracellular glutathione deficiency and exaggerated oxidative stress may contribute to the pathogenesis of fibrosing alveolitis (FA). High-dose N-acetylcysteine (NAC) supplementation partially reverses extracellular glutathione depletion and oxidative damage, but effects on intracellular glutathione are unknown.
Intracellular total glutathione (GSHt) and activation of bronchoalveolar lavage cells (BAC) obtained from 18 FA patients (9 males, aged 52±2 yrs), before and after 12 weeks of oral NAC (600 mg t.i.d.), were assessed. Eight healthy nonsmokers (2 males, aged 36±6 yrs) served as a control group.
Intracellular GSHt was decreased in FA (1.57±0.20 nmol·1x106 BAC1 versus 2.78±0.43 nmol·106 BAC1). After NAC treatment, the intracellular GSHt content increased (1.57±0.20 versus 1.87±0.19 nmol·1x106 BAC1). The spontaneous oxidative activity of BAC decreased after NAC treatment (2.7±0.8 versus 1.0±0.2 nmol·1x106 BAC1·h1). Interleukin-8 concentration (82.1±31.5 versus 80.0±22.6 pg·mL bronchoalveolar fluid (BALF), nonsignificant (ns)) and myeloperoxidase activity (1.93±0.64 versus 1.55±0.47 mU·mL1 BALF, ns) did not change significantly, but were found to be inversely correlated to intracellular GSHt.
In conclusion, high-dose N-acetylcysteine supplementation increases intracellular glutathione levels slightly. This increase is associated with a mild reduction of oxidative activity but not with a reduction of bronchoalveolar cell activation in these patients.
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