Abstract
Valinomycin is a depsipeptide antibiotic which selectively translocates K across biologic membranes. This K ionophore inhibited phytohemagglutinin-stimulated blastogenesis and proliferation in human lymphocytes. The effect was not due to toxicity to the cells nor to the effects of valinomycin as an uncoupler of oxidative phosphorylation. The inhibitory effect on phytohemagglutinin stimulated lymphocytes was prevented by increasing the K concentration of the external media. The interaction of mitogens with specific receptors at the cell membrane apparently may involve mechanisms affecting cation fluxes and membrane potential. These ionic events may play a role in the transduction of membrane signals for lymphocyte stimulation.