Wolpaw E W, Martin D L
Biochim Biophys Acta. 1986 Feb 27;855(2):302-11. doi: 10.1016/0005-2736(86)90178-1.
Transport of SO4(2-) was studied in the glioma cell line LRM55 to determine whether it is mediated by the Cl-/HCO3- exchanger or the K+/Cl- cotransporter previously described in these cells (Wolpaw, E.W. and Martin, D.L. (1984) Brain Res. 297, 317-327). 35SO4(2-) influx was saturable with SO4(2-). External SO4(2-) stimulated 35SO4(2-) efflux, indicating an exchange mechanism. External Cl- was a competitive inhibitor of 35SO4(2-) influx. Internal Cl- stimulated 35SO4(2-) influx and external Cl- stimulated 35SO4(2-) efflux, indicating that Cl- is an exchange substrate for the SO4(2-) carrier. Also, SO4(2-) flux was sensitive to SITS, DIDS and furosemide. However, saturating external SO4(2-) did not inhibit 36Cl- influx and did not inhibit 36Cl- efflux via the Cl-/HCO3- exchanger. Moreover, K+ did not stimulate 36Cl- efflux via the Cl-/HCO3- exchanger. Moreover, K+ did not stimulate 35SO4(2-) influx as it does Cl- influx. These findings indicate that SO4(2-) transport into these cells is mediated by an exchange carrier distinct from both the Cl-/HCO3- exchanger and the K+/Cl- cotransporter. While Cl- is an alternative substrate for the SO4(2-) porter, this carrier is responsible for only a minor fraction of total Cl- flux in these cells.
在神经胶质瘤细胞系LRM55中研究了SO4(2-)的转运，以确定其是否由先前在这些细胞中描述的Cl-/HCO3-交换体或K+/Cl-协同转运体介导（Wolpaw, E.W.和Martin, D.L. (1984) Brain Res. 297, 317 - 327）。35SO4(2-)内流对SO4(2-)具有饱和性。细胞外的SO4(2-)刺激了35SO4(2-)外流，表明存在一种交换机制。细胞外的Cl-是35SO4(2-)内流的竞争性抑制剂。细胞内的Cl-刺激35SO4(2-)内流，细胞外的Cl-刺激35SO4(2-)外流，这表明Cl-是SO4(2-)载体的交换底物。此外，SO4(2-)通量对SITS、DIDS和速尿敏感。然而，饱和的细胞外SO4(2-)并不抑制36Cl-内流，也不抑制通过Cl-/HCO3-交换体的36Cl-外流。此外，K+并不刺激通过Cl-/HCO3-交换体的36Cl-外流。而且，K+不像刺激Cl-内流那样刺激35SO4(2-)内流。这些发现表明，SO4(2-)进入这些细胞的转运是由一种与Cl-/HCO3-交换体和K+/Cl-协同转运体都不同的交换载体介导的。虽然Cl-是SO4(2-)转运体的替代底物，但该载体仅负责这些细胞中总Cl-通量的一小部分。
