Alloxan decreases intracellular potassium content of the isolated frog skin epithelium.

Alloxan has been widely used to provoke diabetes mellitus. This compound induces necrosis of the beta-pancreatic cells and the renal tubules. However, the mechanism of this action has not been fully established. There is some evidence that this drug may act by an alteration of several ionic transport mechanisms. Nevertheless, there is scant information on the effect of alloxan on these ionic transport mechanisms of the membrane in epithelial cells. We reported that this drug induces a decrease in sodium transport in the frog skin. In order to obtain information about the mechanism involved in the sodium transport diminution provoked by alloxan, in this study the function of Na+-K+ ATPase enzyme on transepithelial sodium transport altered by alloxan is explored. We measured changes in the short circuit current and in the intracellular content of sodium and potassium under conditions of maximally stimulated enzyme activity. Short circuit current was not modified by the treatment with alloxan during the period of highest activity of the enzyme, suggesting a site of action independent of this ATPase. Cell potassium was reduced in alloxan-treated epithelia, without significant changes in Na+ content. This finding points out the existence of an alteration induced by alloxan of some modulator mechanisms of the intracellular K+ concentration. The treatment of the frog skin with cesium chloride, a K+ channel blocker, prevented the decrease of Na+ transport produced by alloxan. This result suggests an action of this diabetogenic drug on the K+ channels of the frog skin epithelium.