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首页> 外文期刊>Bioengineering >Tracking Lysosome Migration within Chinese Hamster Ovary (CHO) Cells Following Exposure to Nanosecond Pulsed Electric Fields
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Tracking Lysosome Migration within Chinese Hamster Ovary (CHO) Cells Following Exposure to Nanosecond Pulsed Electric Fields

机译：跟踪纳秒脉冲电场后中国仓鼠卵巢（CHO）细胞内的溶酶体迁移

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Above a threshold electric field strength, 600 ns-duration pulsed electric field (nsPEF) exposure substantially porates and permeabilizes cellular plasma membranes in aqueous solution to many small ions. Repetitive exposures increase permeabilization to calcium ions (Ca 2+ ) in a dosage-dependent manner. Such exposure conditions can create relatively long-lived pores that reseal after passive lateral diffusion of lipids should have closed the pores. One explanation for eventual pore resealing is active membrane repair, and an ubiquitous repair mechanism in mammalian cells is lysosome exocytosis. A previous study shows that intracellular lysosome movement halts upon a 16.2 kV/cm, 600-ns PEF exposure of a single train of 20 pulses at 5 Hz. In that study, lysosome stagnation qualitatively correlates with the presence of Ca 2+ in the extracellular solution and with microtubule collapse. The present study tests the hypothesis that limitation of nsPEF-induced Ca 2+ influx and colloid osmotic cell swelling permits unabated lysosome translocation in exposed cells. The results indicate that the efforts used herein to preclude Ca 2+ influx and colloid osmotic swelling following nsPEF exposure did not prevent attenuation of lysosome translocation. Intracellular lysosome movement is inhibited by nsPEF exposure(s) in the presence of PEG 300-containing solution or by 20 pulses of nsPEF in the presence of extracellular calcium. The only cases with no significant decreases in lysosome movement are the sham and exposure to a single nsPEF in Ca 2+ -free solution.
机译：超过阈值电场强度，持续600 ns持续时间的脉冲电场（nsPEF）暴露，并使水溶液中的细胞质膜透化成许多小离子。重复暴露以剂量依赖性方式增加了对钙离子（Ca 2+）的透化作用。这种暴露条件会产生相对较长寿命的孔，这些孔在脂质被动横向扩散后应重新密封，从而重新封闭了孔。最终进行孔重密封的一种解释是主动膜修复，而哺乳动物细胞中普遍存在的修复机制是溶酶体胞吐作用。先前的研究表明，在5 Hz的20脉冲单列的16.2 kV / cm，600 ns PEF暴露下，细胞内溶酶体运动停止。在该研究中，溶酶体停滞与细胞外溶液中Ca 2+的存在以及微管的塌陷定性相关。本研究检验了以下假设：nsPEF诱导的Ca 2+内流和胶体渗透细胞肿胀的局限性使得溶酶体在裸露细胞中的转运不会减弱。结果表明，本文用于阻止nsPEF暴露后Ca 2+内流和胶体渗透膨胀的努力并未阻止溶酶体易位的减弱。在含PEG 300的溶液中存在nsPEF暴露或在细胞外钙存在下通过20脉冲nsPEF抑制细胞内溶酶体的运动。溶酶体运动没有明显减少的唯一情况是假手术和在不含Ca 2+的溶液中暴露于单一nsPEF。

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