Ravdin J I, Guerrant R L, Sperelakis N
Exp Parasitol. 1985 Aug;60(1):63-72. doi: 10.1016/s0014-4894(85)80023-0.
Entamoeba histolytica, and invasive enteric protozoa, kills mammalian target cells by sequential adherence and cytolytic events. Using platinum plate electrodes with an alternating current source placed in a Wheatstone bridge circuit, the impedance (resistance to ion flow) of a cell suspension of axenic amebae (strain HM1-IMSS) was measured. The impedance of the amebic cell suspension, expressed as resistivity (in ohm-cm), was significantly greater than the test solution and increased with decreasing temperature or greater cell packing (P less than 0.01), indicating that the resistivity measurements reflected the impedance of the amebic surface membrane. Cytochalasin D (10 micrograms/ml), a microfilament inhibitor which inhibited amebic in vitro adherence and cytolysis of target Chinese hamster ovary (CHO) cells (P less than 0.001), also increased resistivity of the amebic suspension (P less than 0.01). Exposure of amebae to bepridil (10(5) M), a slow-channel blocker, inhibited amebic killing of target cells (P less than 0.01) and also increased the resistivity of the amebic suspension (P less than 0.01), but both to a lesser degree than cytochalasin D (P less than 0.001). In contrast, exposure of amebae to verapamil followed by washing had no effect on amebic killing of target cells or resistivity of the amebic suspension. The increased resistivity measured in cytochalasin D or following exposure to bepridil was not due to a change in cell density of the amebic suspension. These studies indicate that changes in impedance of the amebic surface membrane are produced by bepridil and cytochalasin D. The effect of these agents on membrane impedance may contribute directly to the concurrent observed alteration in amebic cytopathogenic capacity or may serve as a parallel marker for the cell membrane alterations induced by such pharmacologic agents which inhibit amebic microfilament function or calcium flux.
溶组织内阿米巴，一种侵袭性肠道原生动物，通过一系列粘附和细胞溶解事件杀死哺乳动物靶细胞。使用置于惠斯通电桥电路中的带有交流电源的铂板电极，测量无菌阿米巴（菌株HM1-IMSS）细胞悬液的阻抗（对离子流动的阻力）。以电阻率（欧姆 - 厘米）表示的阿米巴细胞悬液的阻抗显著大于测试溶液，并随着温度降低或细胞堆积增加而增加（P小于0.01），表明电阻率测量反映了阿米巴表面膜的阻抗。细胞松弛素D（10微克/毫升），一种微丝抑制剂，抑制阿米巴体外对靶中国仓鼠卵巢（CHO）细胞的粘附和细胞溶解（P小于0.001），也增加了阿米巴悬液的电阻率（P小于0.01）。将阿米巴暴露于慢通道阻滞剂苄普地尔（10⁵ M），抑制了阿米巴对靶细胞的杀伤（P小于0.01），也增加了阿米巴悬液的电阻率（P小于0.01），但两者程度均小于细胞松弛素D（P小于0.001）。相比之下，将阿米巴暴露于维拉帕米后冲洗，对阿米巴对靶细胞的杀伤或阿米巴悬液的电阻率没有影响。在细胞松弛素D中或暴露于苄普地尔后测量的电阻率增加并非由于阿米巴悬液细胞密度的变化。这些研究表明，苄普地尔和细胞松弛素D会导致阿米巴表面膜阻抗的变化。这些药物对膜阻抗的影响可能直接导致同时观察到的阿米巴细胞致病能力的改变，或者可能作为此类抑制阿米巴微丝功能或钙通量的药物诱导的细胞膜改变的平行标志物。
