纳秒脉冲电场(nsPEFs)是一种脉冲功率技术，可以消融肿瘤，但它们也调节多种生物机制。在这里我们展示了nsPEFs调控钻透质量膜电子传递速率(tPMET)在质膜还原系统(PMRS)中所示的细胞不透性的WST-8四唑染料的还原。在较低的充电条件下，nsPEFs增强，在较高的充电条件下抑制H9c2非癌性心肌母细胞和4T1-luc乳腺癌细胞的tPMET。这种双相的nsPEF诱导的tPMET调节是一种在较低水平上对身体有益且适应压力，在较高水平上导致损害的荷尔蒙刺激。nsPEFs也减弱了线粒体电子传递系统(ETS)在耦合和解耦氧化磷酸化的Complex I中的活性(氧耗)。相比细胞质(细胞ROS)，nsPEFs在线粒体(mROS)中生成了更多的活性氧物质(ROS)在非癌性心脏细胞H9c2中，但在4T1-luc癌细胞中产生了比mROS更多的细胞ROS。在较低的充电条件下，nsPEFs支持糖酵解，而在较高的充电条件下，nsPEFs抑制PMRS和线粒体ETS中的电子传递，产生ROS，最终导致细胞死亡。nsPEF对ETS的影响为考虑nsPEF调节氧化还原功能，包括氧化还原平衡和新陈代谢提供了一个新的范例。版权所有 © 2023. Elsevier B.V. 出版。

Nanosecond pulsed electric fields (nsPEFs) are a pulsed power technology known for ablating tumors, but they also modulate diverse biological mechanisms. Here we show that nsPEFs regulate trans-plasma membrane electron transport (tPMET) rates in the plasma membrane redox system (PMRS) shown as a reduction of the cell-impermeable, WST-8 tetrazolium dye. At lower charging conditions, nsPEFs enhance, and at higher charging conditions inhibit tPMET in H9c2 non-cancerous cardiac myoblasts and 4T1-luc breast cancer cells. This biphasic nsPEF-induced modulation of tPMET is typical of a hormetic stimulus that is beneficial and stress-adaptive at lower levels and damaging at higher levels. NsPEFs also attenuated mitochondrial electron transport system (ETS) activity (O2 consumption) at Complex I when coupled and uncoupled to oxidative phosphorylation. NsPEFs generated more reactive oxygen species (ROS) in mitochondria (mROS) than in the cytosol (cROS) in non-cancer H9c2 heart cells but more cROS than mROS in 4T1-luc cancer cells. Under lower charging conditions, nsPEFs support glycolysis while under higher charging conditions, nsPEFs inhibit electron transport in the PMRS and the mitochondrial ETS producing ROS, ultimately causing cell death. The impact of nsPEF on ETS presents a new paradigm for considering nsPEF modulation of redox functions, including redox homeostasis and metabolism.Copyright © 2023. Published by Elsevier B.V.