Heavy Metals and Membrane Functions of an Alveolar Epithelium

Abstract

The anuran lung can be mounted as a planar sheet for assessment of bioelectric properties and solute and water permeation. The lung of the bullfrog exhibited a transmural electrical p.d. of 19 mV (pleura positive), a resistance of 700 ohm cm² and a short-circuit current (I_sc) of 27 μa/cm². I_sc reflected active Cl^- secretion into the lumen by a transport mechanism located at the luminal border of the alveolar epithelial cell layer. Other halides and SCN^- were secreted; other bathing solution ions and H₂O followed the predictions for passive diffusion. Exposure of the luminal surface of the lung or disaggregated epithelial cells to heavy metals revealed two patterns of response. HgCl₂ decreased I_sc, cell ciliary motility and Q_O2; CdCl₂ and NiCl₂ inhibited only Q_O2 and cilia. Effects of CdCl₂ were reversed by dimercaprol but not by albumin. SH agents limited but did not reverse HgCl₂ toxicity. None of the metals altered osmotic flow across the lung even though most increased flow across the urinary bladder from the same species. The effects of HgCl₂ on bioelectric properties reflected changes in ion permeation. HgCl₂ followed by a SH compound stimulated I_sc and the pleural to lumen Cl- flux selectively. Without complexer, transient stimulation was followed by a decrease in I_sc and an indiscriminate increase in ion permeability. We conclude that responses to heavy metals separate functions of ciliated cells from Cl^- transport by the non-ciliated epithelium. Furthermore, non-specific cell damage by HgCl₂ can be limited by SH agents to a selective action on the Cl^- pump.