The rates of H₂S and HS^- transport across the human erythrocyte membrane were estimated by measuring rates of dissipation of pH gradients in media containing 250 µM H₂S/HS^-. Net acid efflux is caused by H₂S/HS^- acting analogously to CO₂/HCO₃^- in the Jacobs-Stewart cycle. The steps are: 1) H₂S efflux through the lipid bilayer and/or a gas channel; 2) extracellular H₂S deprotonation; 3) HS^- influx in exchange for Cl^-, catalyzed by the anion exchange protein AE1; 4) intracellular HS^- protonation. Net acid transport by the Cl^-/HS^-/H2S cycle is more efficient than by the Cl^-/HCO₃^-/CO₂ cycle be-cause of the rapid H₂S/HS^- interconversion in both cells and medium. The rates of acid transport were analyzed by solving the mass flow equations for the cycle to produce estimates of the HS^- and H₂S transport rates. The data indicate that HS^- is a very good substrate for AE1; the Cl^-/HS^- exchange rate is about 1/3 as rapid as Cl^-/HCO₃^- exchange. The H₂S permeability coefficient must also be high (>10^-2 cm s^-1; half-time <0.003s) to account for the pH equilibration data. The results imply that 1) H₂S and HS^- enter erythrocytes very rapidly in the microcirculation of H₂S-producing tissues, thereby acting as a sink for H₂S and lowering the local extracellular concentration; and 2) the fact that HS^- is a substrate for a Cl^-/HCO₃^- exchanger indicates that some effects of exogenous H₂S/HS^- may not result from a regulatory role of H₂S but rather from net acid flux by H₂S and HS^- transport in a Jacobs-Stewart cycle.