N-acetylcysteine (600 mg/day) was given to patients by mouth for five days before bronchoscopy and bronchoalveolar lavage to determine whether N-acetylcysteine could increase the concentrations of the antioxidant reduced glutathione in plasma and bronchoalveolar lavage fluid. Bronchoalveolar lavage was performed 1-3 hours (group 2, n = 9) and 16-20 hours (group 3, n = 10) after the last dose of N-acetylcysteine and the values were compared with those in a control group receiving no N-acetylcysteine (group 1, n = 8). N-acetylcysteine was not detected in plasma or lavage fluid. Plasma concentrations of cysteine, the main metabolite of Nacetylcysteine and a precursor of reduced glutathione, were greater in the groups receiving treatment (groups 2 and 3) than in group 1. Cysteine concentrations in lavage fluid were similar in the three groups. Concentrations of reduced glutathione were greater in both plasma and lavage fluid in group 2 than in group 1. These data suggest that Nacetylcysteine given by mouth is rapidly deacetylated to cysteine, with resulting increases in the concentrations of cysteine in plasma and of reduced glutathione in plasma and the airways, which thus temporarily increase the antioxidant capacity of the lung.

Background -Oxidant/antioxidant imbalance may occur in the lungs of patients with chronic obstructive pulmonary disease (COPD). Glutathione is an important extracellular and intracellular thiol oxidant in the lungs. These studies were carried out to determine the effect of N-acetyl cysteine on thiol concentrations in plasma, bronchoalveolar lavage fluid, and lung tissue. Methods -Studies were carried out on normal subjects, patients with COPD, and those undergoing lung resection. In

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Acute cigarette smoking increases the sequestration of neutrophils in the lungs of humans. This may be due to the delayed transit of cells in the pulmonary microcirculation, which may result from a reduction in cell deformability as suggested by in vitro studies of smoke-exposed neutrophils. In order to support this hypothesis we wished to determine if a reduction in leukocyte deformability could be measured in whole blood exposed to smoke in vitro or in vivo. Whole blood filterability, which largely reflects leukocyte deformability, was measured as the pressure developed by filtration of diluted whole blood through a micropore membrane. Whole blood filtration pressures did not change when blood was exposed to smoke in vitro or in venous blood after acute smoking in vivo. However, arterial blood sampled from chronic smokers during acute smoking showed a consistent reduction in leukocyte deformability associated with a small increase in plasma elastase. To assess whether these changes were induced by oxidants in cigarette smoke, we measured the levels of the antioxidant glutathione (GSH), erythrocyte (RBC) membrane fragility, and products of lipid peroxidation in plasma and RBC in blood exposed to smoke in vivo and in vitro. No change in RBC lipid peroxidation or membrane fragility could be detected after in vitro smoke exposure, possibly because of the high antioxidant capacity of the RBC. However, reduced blood GSH levels and increased levels of lipid peroxidation products were detected in plasma, reflecting oxidant stress. In contrast, we were unable to detect evidence of an increased oxidant burden in blood after acute smoking in vivo, in either arterial or venous blood samples.(ABSTRACT TRUNCATED AT 250 WORDS)