The transport of [ 14 C]oxalate (Ox 2-) by epithelial brushborder membrane vesicles (BBMV) of lobster (Homarus americanus) hepatopancreas, formed by a magnesium precipitation technique, was stimulated by an outward Clgradient (in > > out). By contrast, Ox 2-uptake was not enhanced by an inward Na + or K + transmembrane gradient. Generation of an inside-positive membrane potential by K + in the presence of valinomycin stimulated Ox 2-/Cl -exchange, while an inside-negative membrane potential generated by K + efflux in the presence of valinomycin inhibited this process. Neither Ox 2-/Ox 2-nor Ox 2-/SO4 2-transport exchange were affected by alterations of transmembrane potential. An inwardly directed proton gradient, or the presence of low bilateral pH, enhanced Ox 2-/Cl -exchange, yet the H + gradient alone could not stimulate Ox 2-uptake in Cl --equilibrated BBMV or in vesicles lacking internal Cl -. The stilbenes 4-acetamido-4′ ′-isothiocyanotostilbene-2,2′ ′-disulfonic acid (SITS) and 4,4′ ′-diisothiocyano-2,2′ ′-disulfonic stilbene (DIDS) strongly inhibited Ox 2-/Cl -exchange. Oxalate influx occurred by a combination of carrier-mediated transfer, exhibiting Michaelis-Menten kinetics, and nonsaturable 'apparent diffusion'. Apparent kinetic constants for Ox 2-/Cl -exchange were Kt=0.20·mmol·l -1 and Jmax=1.03·nmol·l -1 ·mg -1 ·protein·7·s -1 . 36 Cl -influx into oxalate-loaded BBMV was stimulated by an insidenegative transmembrane potential compared with shortcircuited vesicles. These results suggest that Ox 2-/Clexchange in crustacean hepatopancreatic BBMV occurred by an electrogenic carrier mechanism exhibiting a 1:1 flux ratio that was modulated by an external proton-sensitive regulatory site.