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AIM:To investigate the type of chloride channel activated by cisplatin in poorly differentiated na -sopharyngeal carcinoma cells (CNE-2Z cells).METHODS:The technique of whole-cell patch-clamp was used to investi-gate the role of Ca 2+in the activation of cisplatin-activated chloride currents and to analyze the effect of hypertonic stress on these currents in CNE-2Z cells.RESULTS:Chloride currents were induced when the cells were exposed to the calcium -free cisplatin solution , showing the similar density to the currents induced by cisplatin with the presence of extracellular cal -cium.However , the latency and the peak time of cisplatin-activated currents in the absence of extracellular calcium were prolonged.The activation of cisplatin-activated chloride currents was insensitive to the depletion of intra-and extracellular calcium.Calcium channel antagonist nifedipine had no effect on the cisplatin -activated chloride currents , while hypertonic solution completely inhibited those currents .CONCLUSION:The cisplatin-activated chloride currents are independent on intra/extracellular calcium .The chloride channels activated by cisplatin are not calcium-activated chloride channels , but are probably volume-sensitive chloride channels .
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gluconate in both G1 phase and S phase cells.The permeability of G1 phase cells to I-was higher than that in S phase cells,but to gluconate was lower than that in S phase cells.CONCLUSIONS: The density of the volume-activated Cl-current,the anion permeability of the channel and the sensitivity of the current to tamoxifen were different between the CNE-2Z cells in G1 phase and those in S phase.The results suggest that the expression of tamoxifen-sensitive,volume-activated chloride channels is differentiated at different stages of the cell cycle.
