Frank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
Bioelectrochemistry. 2011 Oct;82(2):131-4. doi: 10.1016/j.bioelechem.2011.06.002. Epub 2011 Jun 16.
We investigated the effects of nanosecond pulsed electric fields (nsPEF) on three human cell lines and demonstrated cell shrinkage, breakdown of the cytoskeleton, nuclear membrane and chromosomal telomere damage. There was a differential response between cell types coinciding with cell survival. Jurkat cells showed cytoskeleton, nuclear membrane and telomere damage that severely impacted cell survival compared to two adherent cell lines. Interestingly, disruption of the actin cytoskeleton in adherent cells prior to nsPEF exposure significantly reduced cell survival. We conclude that nsPEF applications are able to induce damage to the cytoskeleton and nuclear membrane. Telomere sequences, regions that tether and stabilize DNA to the nuclear membrane, are severely compromised as measured by a pan-telomere probe. Internal pore formation following nsPEF applications has been described as a factor in induced cell death. Here we suggest that nsPEF induced physical changes to the cell in addition to pore formation need to be considered as an alternative method of cell death. We suggest nsPEF electrochemical induced depolymerization of actin filaments may account for cytoskeleton and nuclear membrane anomalies leading to sensitization.
我们研究了纳秒级脉冲电场（nsPEF）对三种人类细胞系的影响，结果表明细胞收缩、细胞骨架、核膜和染色体端粒损伤。细胞类型之间存在与细胞存活相关的差异反应。与两种贴壁细胞系相比，Jurkat 细胞表现出明显的细胞骨架、核膜和端粒损伤，严重影响细胞存活。有趣的是，在 nsPEF 暴露之前破坏贴壁细胞中的肌动蛋白细胞骨架会显著降低细胞存活率。我们得出结论，nsPEF 应用能够诱导细胞骨架和核膜损伤。端粒序列是将 DNA 固定到核膜上的区域，通过全端粒探针测量，端粒序列严重受损。nsPEF 应用后形成的内部孔已被描述为诱导细胞死亡的因素之一。在这里，我们建议除了孔形成之外，还需要考虑 nsPEF 诱导的细胞物理变化作为细胞死亡的另一种方法。我们建议 nsPEF 电化学诱导的肌动蛋白纤维解聚可能导致细胞骨架和核膜异常，从而导致敏化。
