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Halide transport in Xenopus oocytes.

1. Radioisotopes and intracellular microelectrodes were used to characterize the permeability of Xenopus oocytes to chloride and other halides. 2. Uptake of 36Cl had a half‐time for equilibration of approximately 3 h, with an initial rate of Cl‐ entry corresponding to a permeability coefficient of 3.9 x 10(‐7) cm/s, and an equilibrium uptake of 36Cl of 33 mM. 3. Replacement of bathing Na+ by K+ depolarized the oocytes from ‐46 to ‐7 mV and stimulated influx approximately 3‐fold. 4. Influx was linearly dependent on bathing [Cl‐] and was temperature dependent with an activation energy of 46 kJ/mol. Influx of 125I of 36Cl was not affected by the presence of equal concentrations of other halides or thiocyanate. These results are consistent with a channel‐mediated entry mechanism. 5. Diphenylamine‐2‐carboxylate (DPAC) and 9‐anthracene carboxylate (9‐AC), blockers of Cl‐ channels in other cells, inhibited Cl‐ entry with dissociation constants (Kds) of approximately 5 x 10(‐4) and approximately 10(‐3) M, respectively. Inhibitors of Cl(‐)‐HCO3‐ exchange or Na(+)‐K(+)‐2Cl‐ co‐transport did not affect Cl‐ influx. 6. Attempts to lower or raise intracellular Ca2+ with BAPTA or A23187, respectively, were also without effect on Cl‐ influx. 7. The halide selectivity sequence determined with isotopes was I‐ (3.2) greater than Br‐ (1.3) greater than Cl‐ (1.0). However, DPAC inhibited almost all of the 36Cl influx but only a small fraction of 125I influx. 8. Replacement of bathing Cl‐ by I‐ or Br‐resulted in hyperpolarizations, from which the same selectivity sequence was determined. 9. Replacement of bathing Cl‐ by gluconate caused a marked depolarization, which was inhibited by DPAC and, less potently, by 9‐AC.