The sulfhydryl reagent thimerosal at concentrations 5-100 μM has been found to induce a variety of changes in ion transport in rat thymocytes. In particular, [Ca2+]iincreases about 10-fold from the basal level. The [Ca2+]iresponse to thimerosal displays a two-stage time course, with the main [Ca2+]irise during the second stage. Evidence has been obtained for the depletion of intracellular Ca2+pools in thimerosal-treated cells, however, Ca2+mobilization from intracellular stores does not contribute significantly into [Ca2+]irise. Thimerosal elicits permeability not only for Ca2+, but also for Mn2+and Ni2+, which is Ca2+-dependent. We failed to get any evidence on thimerosal-induced inhibition of the plasma membrane Ca2+-ATPase. The induction of Ca2+influx, rather than inhibition of Ca2+-ATPase, accounts for the disturbance of [Ca2+]ihomeostasis in thimerosal-treated cells. Thimerosal also elicits changes in monovalent ion fluxes resulting in marked depolarization. The latter seems unrelated to the changes in [Ca2+]iand is suggested to be mediated both by increased permeability for Na+and a decreased one for K+. Thimerosal significantly stimulates AA release from thymocytes. Evidence has been presented that AA metabolite(s), probably, LO product(s), may mediate the changes in the transport of mono- and divalent cations elicited by the sulfhydryl reagent. Prolonged treatment of thymocytes with thimerosal resulted in cell death. © 1992.