Disturbances in Na+ transport systems induced by ethanol in human red blood cells

Abstract

The effects of ethanol on fluxes catalyzed by four Na+ transport systems (ouabain-sensitive Na+, K+ pump, bumetanide-sensitive Na+, K+ cotransport system, Na+:Li+- countertransport and anion carrier) and on Na+ and K+ leaks were investigated in human red blood cells. Ethanol concentrations higher than 32 mM were required in order to significantly modify erythrocyte Na+ transport function. The observed changes can be summarized as follows: (a) stimulation of Na+ efflux through the Na+, K+ pump (by 21-32% at 160-400 mM) and Na+:Li+ countertransport (by 34-59% at 160-400 mM); (b) inhibition of outward Na+, K+ cotransport (by 23-34% at 160-400 mM) and LiCO3- influx through the anion carrier (by 17-21% at 64-400 mM); and (c) increase in Na+ and K+ leaks (by 13-16% at 64-400 mM). The effects of ethanol on the Na+,K+ pump and Na+,K+ cotransport system resulted from changes in maximal rates of Na+ efflux (increased and decreased, respectively) without any significant effect on the apparent affinities for internal Na+. Erythrocytes preincubated for 1 hr with 160 mM ethanol, washed and further incubated in flux media, recovered a normal Na+ transport function. In conclusion, high concentrations of ethanol induced reversible perturbations of fluxes catalyzed by erythrocyte Na+ transport systems. The observed effects may reflect disturbances in Na+ transport function associated with severe intoxication.