Na and K transport provoked in Ehrlich ascites tumor cells by addition of arachidonic acid is via conductive ion channels and not via any Na<sup>+</sup>/H<sup>+</sup> or K<sup>+</sup>/H<sup>+</sup> exchange systems nor any Cl-dependent cotransport system. The effect of arachidonic acid on the Na conductance is partly mediated via cyclooxygenase metabolites, while the effect on the K conductance is dominantly a nonspecific detergent effect of an unsaturated fatty acid. Ehrlich cells depolarize after transfer to hyptonic media. This depolarization of the cell membrane potential, caused by opening of Cl channels, is completely abolished by arachidonic acid, and cells already depolarized by osmotic swelling hyperpolarize after addition of arachidonic acid. From measured values of Cl net efflux and membrane potentials it is estimated that the increase in Cl conductance in hypotonic medium is significantly inhibited in the presence of arachidonic acid. In isotonic medium, arachidonic acid, on the contrary, seems to increase the basal Cl conductance. It is proposed that, although arachidonic acid in general increases conductive cation and anion transport in Ehrlich ascites tumor cells, it directly inactivates the Cl channel activated by osmotic cell swelling.