## 1 Introduction  
Crossing the lipid cell membrane, a physical barrier separating the intracellular from the extracellular environment, is challenging for laboratory and clinical practice. However, the supply of specific molecules and medicaments to particular cells is fundamental for most treatment pathways [1; 2]. For this reason, medicine is trying to design drugs to allow their active ingredients to connect with the plasma membrane or cross it, thereby influencing particular signaling pathways. The selectivity of the barrier challenges healthcare, especially regarding effective gene delivery. Plenty of nonviral techniques, although safer than the vectors, in past years have resulted in unsatisfactorily low levels of gene delivery and expression in contradistinction to their viral equivalents [3]. The development of EP shed light on a described problem, serving us with a novel, highly effective strategy for transporting molecules into living cells [4]. Electroporation induces transient pore formation in the cell membrane using high-voltage, short-duration electric pulses, which allow the molecules of drugs or nucleic acids to enter the intracellular environment [5]. The described method is characterized by a wide range of advantages, within which we are able to enumerate its universality, simplicity, and efficacy. For instance, when it comes to introducing DNA to the cell cytoplasm, the employment of EP guarantees a lower rate of its mutation as the molecule is not exposed to an endosomal and lysosomal acid environment, which would affect it in any other method [6; 7; 8; 9]. Trying to understand the mechanism that underlays the phenomenon of electroporation and discovering its difficulty is inevitable. As the transformations of the plasma membrane structure during EP are not macroscopically substantial, the mechanism of the described process might seem unclear. Transmembrane voltage changes from physiological (which amounts to approximately 0.1 V) to 0.5-1 V, which leads to the formation of indentation and then transient hydrophobic pores, the diameter of which ranges from 2 to several nanometers [10; 11]. As the transmembrane voltage increases, maintaining hydrophobic pores is energetically more expensive than maintaining hydrophilic pores, which results in the fact that some hydrophobic pores are transmutable into hydrophilic ones. A molecular mechanism that underlays mentioned transition includes reorienting the polar headgroups of lipids towards water molecules [12; 13] (Figure 1). The use of a transmembrane electric field in the range of 0.5 V/nm to 1.0 V/nm induces EP of the lipid bilayer, manifested by the formation of water channels. While at 0.5 V/nm the first water fingers develop within a nanosecond, the same process is much faster (200 ps) for a 1.0 V/nm run. The formation of water fingers penetrates the bilayer hydrophobic core from either side when the bilayer is subject to a transverse electric field. As long as the electric field is present, water fingers expand toward the opposite interface or join other water fingers to form a mature pore that extends from one interface to the other of the bilayer hydrophobic core. This causes the reorganization of lipids. Polar lipid head groups migrate from the membrane-water interface to the interior of the bilayer, forming hydrophilic pores that surround and stabilize the water columns [14; 15]. Ensuring change is the foundation of sustaining the transport after the voltage reverts to its physiological value, as novel pores have extended half-life value and can be stabilized by connection to the cytoskeleton [16; 17; 18; 19; 20; 21]. The lifetime of pores is very short; therefore, recclosing these pores seems arbitrary and can be prolonged while the cells are kept at 0 \({}^{\circ}\)C [6]. Not only does electrical stimulus induce the formation of pores, but also it influences single membrane lipids properties.