Abstract
Hydrogen sulfide (H2S) is well known as a highly toxic environmental chemical threat. Prolonged exposure to H2S can lead to the formation of pulmonary edema. However, the mechanisms of how H2S facilitates edema formation are poorly understood. Since edema formation can be enhanced by an impaired clearance of electrolytes and, consequently, fluid across the alveolar epithelium, it was questioned whether H2S may interfere with transepithelial electrolyte absorption. Electrolyte absorption was electrophysiologically measured across native distal lung preparations (Xenopus laevis) in Ussing chambers. The exposure of lung epithelia to H2S decreased net transepithelial electrolyte absorption. This was due to an impairment of amiloride-sensitive sodium transport. H2S inhibited the activity of the Na+/K+-ATPase as well as lidocaine-sensitive potassium channels located in the basolateral membrane of the epithelium. Inhibition of these transport molecules diminishes the electrochemical gradient which is necessary for transepithelial sodium absorption. Since sodium absorption osmotically facilitates alveolar fluid clearance, interference of H2S with the epithelial transport machinery provides a mechanism which enhances edema formation in H2S-exposed lungs.
Highlights
Hydrogen sulfide (H2S), a gas with the typical smell of rotten eggs, is well known as a highly toxic environmental chemical threat
We have recently shown that exogenously applied H2S decreases Na+ transport across a monolayer of a pulmonary epithelial cell line (H441) [12]
We demonstrate that exposure of these native lung epithelia to H2S decreases the rate of Na+ absorption due to an impairment of the Na+/K+-ATPase as well as K+ channels in the basolateral membrane of pulmonary epithelial cells
Summary
Hydrogen sulfide (H2S), a gas with the typical smell of rotten eggs, is well known as a highly toxic environmental chemical threat. The high toxicity of H2S is, amongst other things, related to the fact that it is inhaled and can cross the alveolo-capillary barrier and is rapidly distributed within the human body [1]. The pulmonary epithelium is the first cell layer which is exposed to H2S. Epithelial cells have been recently shown to have a high capacity to metabolize H2S [2], exposure to high concentrations of H2S (.500 ppm) can lead to severe lung irritation [3]. Prolonged exposure to H2S (250–500 ppm) can impair the barrier function of the alveolar epithelium and lead to the formation of pulmonary edema in humans [3]. Pulmonary edema occurs in mice after exposure to H2S concentration .50 ppm [4]
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