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Nebulized Glutathione Induces Bronchoconstriction in Patients with Mild Asthma
RAMON M. MARRADES, JOSEP ROCA, JOAN ALBERT BARBERÀ, LLUÍS de JOVER, WILLIAM MacNEE, and ROBERT RODRIGUEZ-ROISIN
Am J Respir Crit Care Med 1997;156:425–430.
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To assess the effects on bronchial responsiveness of nebulized glutathione (GSH), one of the most efficient scavengers of oxidant substances in the airways, we studied eight patients with mild asthma (FEV1 , 88 +/- 11% predicted [SD]) in a randomized, double-blind, cross-over, placebo-controlled fashion. Bronchial challenge was measured using both FEV1 and total pulmonary resistance (Rrs) by the forced oscillation technique. Patients received nebulized GSH (600 mg with 4 ml of 0.9% sodium chloride) or placebo (identical saline solution) over a period of 25 min, 1 wk apart. Placebo provoked subclinical mild bronchoconstriction (changes from baseline: FEV1, -1%; Rrs, + 17%); by contrast, GSH caused major airway narrowing (changes from baseline: FEV1 ,-19%; Rrs,+ 61%) and
induced cough (four patients) or breathlessness (three patients). Differences between placebo and GSH after challenge were also noticeable in both FEV1 (p = 0.03) and Rrs (p= 0.02). Neither osmolarity (660 mosm  kg -1 ) nor pH (3.0) of the GSH solution accounted for these effects. Nebulized salbutamol (5.0 mg) given before the GSH challenge blocked GSH-induced bronchoconstriction. Furthermore, GSH-induced FEV 1 falls were inversely correlated with metabisulfite bronchoprovocation (provocative dose [PD20], 1.49 +/- 1.83  μmol) but not with methacholine challenge. The detrimental effects of nebulized GSH on the airway bronchial tone in patients with mild asthma strongly suggests bronchoconstriction provoked by sulfite formation.

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