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Modulation of pneumotoxicity by cellular glutathione and precursors.

The maintenance of intracellular glutathione levels is essential for both the normal functioning of cells and their protection from both intra- and extracellularly derived oxidative damages. As the lungs are exposed both to airborne reactive xenobiotic agents and to inflammatory stress, which may cause severe localized depletions of intracellular glutathione (GSH) with resultant pathological changes, we have studied the potential of the drug N-acetylcysteine (NAC) as a pneumoprotective agent both in vitro and in vivo. These studies have demonstrated that, depending upon the route of administration, NAC may elicit pneumoprotection through a number of distinct mechanisms. NAC may protect cellular integrity by competing with intracellular GSH and reacting directly with potentially toxic agents by spontaneous conjugation and/or reduction. However, when NAC is given orally, in doses similar to those currently used in the treatment of chronic obstructive airways disease, its poor bioavailability, due probably to extensive first-pass metabolism, makes it unlikely that it is available to organs such as the lung for direct scavenging activity. Despite this, oral NAC may elicit pneumoprotection through a 'prodrug' mechanism, supporting circulatory GSH levels through extensive metabolism to cysteine in the gut. This effect may mimic existing homeostatic mechanisms for the control of circulatory GSH levels during peripheral inflammation.