CAJ | 학술논문

目的：探讨顺铂激活的低分化鼻咽癌细胞（ CNE-2Z）氯通道电流是否为钙激活的氯电流。方法：采用膜片钳全细胞记录技术记录细胞内／外无Ca2＋及钙通道阻断剂对顺铂激活氯电流的影响，并用高渗灌流液观察顺铂激活氯电流的容积敏感性。结果：去除细胞外液的Ca2＋后，5μmol／L顺铂能诱发氯电流，且电流大小与细胞外有Ca2＋时无明显差异，但潜伏期与达峰时间延长。细胞内外均无Ca2＋对顺铂激活氯电流未产生影响。钙通道阻断剂nifedipine未能抑制顺铂诱发的氯电流。但细胞外灌流高渗液几乎可完全抑制顺铂激活的氯电流。结论：顺铂激活的氯通道开放不依赖于细胞内／外的Ca 2＋，该通道不是钙激活氯通道而很可能是容积敏感性氯通道。
목적：탐토순박격활적저분화비인암세포（ CNE-2Z）록통도전류시부위개격활적록전류。방법：채용막편겸전세포기록기술기록세포내／외무Ca2＋급개통도조단제대순박격활록전류적영향，병용고삼관류액관찰순박격활록전류적용적민감성。결과：거제세포외액적Ca2＋후，5μmol／L순박능유발록전류，차전류대소여세포외유Ca2＋시무명현차이，단잠복기여체봉시간연장。세포내외균무Ca2＋대순박격활록전류미산생영향。개통도조단제nifedipine미능억제순박유발적록전류。단세포외관류고삼액궤호가완전억제순박격활적록전류。결론：순박격활적록통도개방불의뢰우세포내／외적Ca 2＋，해통도불시개격활록통도이흔가능시용적민감성록통도。
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 .