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Sulfate transport in human lung fibroblasts (IMR‐90)
Author(s) -
Elgavish Ada,
Smith Jeffrey B.,
Pillion Dennis J.,
Meezan Elias
Publication year - 1985
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041250211
Subject(s) - sulfate , chemistry , bicarbonate , extracellular , biochemistry , efflux , chloride , biophysics , biology , organic chemistry
Abstract Sulfate transport in a fibroblast cell line derived from human lung (IMR‐90) occurred mainly via high‐ and low‐affinity, SITS‐sensitive pathways and to a lesser extent by an SITS‐insensitive mechanism. In low‐ionic‐strength media (sucrose substituted for salts) the apparent Km of the carrier‐mediated sulfate influx was 1 mM. At 0.3 mM, the sulfate concentration normally found in human serum, the contribution of the SITS‐insensitive pathway was negligible. In physiological salts solution, an SITS‐sensitive, high‐affinity (Km 34 ± 14 μM) sulfate influx system was observed at extracellular sulfate concentrations less than 100 μM. Between 100 and 500 μM sulfate, the range normally found in human serum, sulfate influx occurred via an SITS‐insitive, lowaffinity pathway and to a small extent by an SITS‐insensitive mechanism. Extracellular chloride inhibited the influx and stimulated the efflux of sulfate. Bicarbonate and thiosulfate inhibited sulfate influx but had no effect on sulfate efflux. Phosphate, arsenate, or Na + did not affect sulfate uptake. These results indicate that in human lung fibroblast IMR‐90 cells sulfate is transported mainly via an SO 4 2− /Cl‐ exchange system independent of the phosphate or Na + transport. Since sulfate concentration as high as 50 mM only slightly increased sulfate efflux, SO 4 2− /SO 4 2− exchange is probably a minor component of sulfate uptake.