It was previously documented that adenosine-stimulated anion secretion in airway epithelia is largely mediated by chloride transport [17, 29] . To explore if the alcohol-suppressed I SC , as identified above, is actually a chloride current, we first confirmed chloride transport by Calu-3 epithelia in our experimental setting. To this end, the cultured Calu-3 epithelia without any alcohol exposure were subjected to I SC measurement in the presence of various inhibitors to block different ion channels. Bumetanide (100 mM), a specific inhibitor for the Na + -K + -2Cl 2 cotransporter, was applied to the basolateral side of the Calu-3 epithelia after adenosine stimulation. This drug decreased I SC by ,58%, while acetazolamide, a carbonic anhydrase inhibitor, and DNDS, an inhibitor for Na + /HCO 3 2 cotransporters and Cl 2 /HCO 3 2 exchangers, had no effect on I SC (Fig. 2A) . These data suggest that the adenosine-stimulated anion current that is suppressed by alcohol is the chloride channel conductance. The result was further validated by measuring the adenosine-stimulated I SC with identical apical and basal chloride buffers. Without chloride gradient (Fig. 2B) , adenosine-induced I SC was dropped significantly by Student's t-test (p,0.01, n = 5). The I SC was only ,8% of that measured with the asymmetric chloride buffers.