Summary
1. The aim of this study was to elucidate if the K+ uptake was higher in cultured human glioma cells than in cells from other malignant tumors and to analyze the importance of membrane potential and K+ channels for the uptake.
2. K+ transport properties were studied with the isotopes42K and the K-analogue201Tl.
3. Comparison with cultured cells from other malignant tumors showed that the specific steady-state accumulation of Tl+ was significantly higher in glioma cells (U-251MG and Tp-378MG).
4. In Ringer's solution at 37°C the rates of K+ and Tl+ uptake were both inhibited by about 55% in ouabain and 60% in furosemide, bumetanide, or Na+-or Cl−-free medium. This indicated that the routes for K+ and Tl+ uptake were similar and due to Na,K-ATPase-dependent transport and to Na-K-Cl cotransport.
5. About 10% of the uptake was neither ouabain nor bumetanide sensitive. Ba2+, which is known to block inward-rectifying K+ channels and to depolarize glial cells, and other K+ channel blockers (Cs+ and bupivacaine), had no effect on Tl+ uptake.
6. Metabolic inhibition with dinitrophenol reduced the uptake rate to 17%.
7. The washout of Tl+ was unaffected by bumetanide and K+ channel blockers, but dinitrophenol caused a transient increase of 75%, an effect which persisted in the presence of K+ channel blockers.
8. It was concluded that the high specific K+ and Tl+ accumulation in cultured human glioma cells was due not to the presence of inwardly rectifying K+ channels or other identified K+ channels, but to Na,K-ATPase dependent transport and Na-K-Cl cotransport.
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Brismar, T., Anderson, S. & Collins, V.P. Mechanism of high K+ and Tl+ uptake in cultured human glioma cells. Cell Mol Neurobiol 15, 351–360 (1995). https://doi.org/10.1007/BF02089945
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DOI: https://doi.org/10.1007/BF02089945