Control of membrane permeability by external ATP in mammalian cells: isolation of an ATP-resistant variant from Chinese hamster ovary cells.
External ATP causes a great increase in the passive permeability of the plasma membrane for phosphorylated metabolites and other small molecules in cultured mammalian cells. We previously demonstrated that in CHO-K1 cells an ATP-dependent permeability change was induced in the presence of a mitochondrial inhibitor (KCN or rotenone), a cytoskeleton-attacking agent (vinblastine) and a calmodulin antagonist (trifluoperazine). These permeability changes were reversible but long exposure, for 30-60 min, to ATP together with a mitochondrial inhibitor significantly reduced the cell viability of the treated cells. Since this cell lysis was shown to be due to the ATP-dependent permeability change, we could isolate several clones resistant to the action of the external ATP from CHO-K1 cells after repeated treatment with ATP and rotenone. In 9.1 cells, one of the isolated clones, little or no ATP-dependent permeability change was observed in the presence of either a mitochondrial inhibitor, vinblastine or trifluoperazine. This CHO variant could be specifically resistant as to the change in membrane permeability induced by external ATP, since the permeabilities for the 2-deoxyglucose and drugs used in the present studies were similar to those in the case of the parent cells. These results suggest that a specific defect or alteration in the plasma membrane is involved in the ATP-dependent permeability change. It is also reported that Mg2+-dependent ATPase activity was found on the cell surface of both CHO-K1 and 9.1 cells, and this activity was shown to be not involved in the permeability change controlled by external ATP.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism; D002460:Cell Line; D002463:Cell Membrane Permeability / Q000187:drug effects*; D006224:Cricetinae; D003847:Deoxyglucose / Q000378:metabolism; D004351:Drug Resistance; D005260:Female; D007700:Kinetics; D010053:Ovary; D011190:Potassium Cyanide / Q000494:pharmacology; D012402:Rotenone / Q000494:pharmacology; D014268:Trifluoperazine / Q000494:pharmacology; D014747:Vinblastine / Q000494:pharmacology
D012402:Rotenone; D014268:Trifluoperazine; D014747:Vinblastine; D000255:Adenosine Triphosphate; D003847:Deoxyglucose; D017301:Ca(2+) Mg(2+)-ATPase; D011190:Potassium Cyanide