Control of membrane permeability to exogenous compounds by membrane electroporation can lead to cell death, which is related to permanent membrane damage, oxidation stress, leakage of intracellular molecules. In this study, we show that the predominant cell death modality after the application of high voltage electric pulses is related with inability to reseal of initial pores (first stage irreversible electroporation, FirEP). After moderately strong electric pulses, initial pores reseal, however, some cell still die later on due to electric field induced cell stress which leads to delayed cell death (late-stage irreversible electroporation, LirEP). According to our data, the period in which the majority of cells commit to either pore resealing or complete loss of barrier function depends on the intensity of electric field treatment but did not exceed 35 min. Additionally, we show that after electroporation using electric pulse parameters that induce LirEP, some cells can be rescued by supplementing medium with compounds obtained from irreversibly electroporated cells. We determined that the intracellular molecules that contribute to the increase of cell viability are larger than 30 kDa. This serves to prove that the loss of intracellular compounds plays a significant role in the decrease of cell viability after electroporation.

通过膜电穿孔控制膜对外源性化合物的渗透性可导致细胞死亡，这与永久性膜损伤，氧化应激，细胞内分子泄漏有关。在这项研究中，我们表明，施加高压电脉冲后，主要的细胞死亡方式与无法重新密封初始毛孔（第一阶段不可逆电穿孔，FirEP）有关。经过中等强度的电脉冲后，最初的毛孔重新密封，但是，由于电场诱导的细胞应力而导致细胞死亡延迟（后期不可逆电穿孔，LirEP），一些细胞仍在以后死亡。根据我们的数据，大多数细胞致力于孔重密封或完全丧失屏障功能的时间取决于电场处理的强度，但不超过35分钟。此外，我们显示使用诱导LirEP的电脉冲参数进行电穿孔后，可以通过向培养基中添加从不可逆电穿孔细胞中获得的化合物来拯救某些细胞。我们确定，有助于细胞活力增加的细胞内分子大于30 kDa。这证明了细胞内化合物的损失在电穿孔后细胞活力的降低中起着重要作用。通过向培养基中添加从不可逆电穿孔细胞中获得的化合物，可以拯救某些细胞。我们确定，有助于细胞活力增加的细胞内分子大于30 kDa。这证明了细胞内化合物的损失在电穿孔后细胞活力的降低中起着重要作用。通过向培养基中添加从不可逆电穿孔细胞中获得的化合物，可以拯救某些细胞。我们确定，有助于细胞活力增加的细胞内分子大于30 kDa。这证明了细胞内化合物的损失在电穿孔后细胞活力的降低中起着重要作用。