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首页> 外文期刊>Cellular Physiology and Biochemistry >Stimulation of Suicidal Erythrocyte Death by Benzethonium
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Stimulation of Suicidal Erythrocyte Death by Benzethonium

机译：苄索溴铵刺激自杀性红细胞死亡

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Benzethonium, an antimicrobial surfactant widely used as preservative of pharmaceuticals, topical wound care product and oral disinfectant, triggers apoptosis of several cell types. The apoptosis is preceded and possibly triggered by mitochondrial depolarization. Even though lacking mitochondria, erythrocytes may similarly undergo suicidal cell death or eryptosis. Hallmarks of eryptosis include cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptosis may be triggered by energy depletion, which leads to increase of cytosolic Casup2+/sup-activity with subsequent Casup2+/sup-sensitive cell shrinkage and cell membrane scrambling. Casup2+/sup-sensitivity is enhanced by ceramide. The present study explored the effect of benzethonium on eryptosis. Cell membrane scrambling was estimated from binding of fluorescent annexin V to phosphatidylserine, cell volume from forward scatter in FACS analysis, cytosolic Casup2+/sup-concentration from Fluo3-fluorescence, hemolysis from hemoglobin release, lactate formation by colorimetry and ceramide utilizing fluorescent antibodies. A 48 hours exposure to benzethonium (=5µM) significantly increased cytosolic Casup2+/sup-concentration, decreased forward scatter and triggered annexin V-binding affecting some 30% of the erythrocytes at 5 µM benzethonium. Only 5% of treated erythrocytes were hemolytic. The effects of benzethonium on annexin V binding were blunted in the nominal absence of Casup2+/sup and in the presence of amiloride (1 mM) but not in the presence of the pancaspase inhibitor zVAD (10 µM). Benzethonium further significantly enhanced the effect of glucose depletion on cytosolic Casup2+/sup-concentration and annexin V-binding, but significantly blunted the effect of glucose depletion on forward scatter. Benzethonium (5 µM) significantly enhanced lactic acid formation but not ceramide abundance. The present observations disclose a novel effect of benzethonium, i.e. triggering of suicidal death of erythrocytes.
机译：苯并鎓是一种广泛用作药物，局部伤口护理产品和口腔消毒剂的防腐剂的抗微生物表面活性剂，可触发多种细胞类型的凋亡。凋亡发生在线粒体去极化之前，并可能由线粒体去极化触发。即使缺乏线粒体，红细胞也可能类似地发生自杀性细胞死亡或隐匿。加密的标志包括细胞收缩和在细胞表面暴露有磷脂酰丝氨酸的细胞膜争夺。能量消耗可能触发了加密作用，导致细胞溶质中Ca 2 + 的活性增加，随后Ca 2 + 敏感的细胞收缩和细胞膜混乱。神经酰胺可增强Ca 2 + 的敏感性。本研究探索了苄索溴铵对密码作用的影响。通过荧光膜联蛋白V与磷脂酰丝氨酸的结合，FACS分析中前向散射的细胞体积，Fluo3-荧光的胞浆Ca 2 + 浓度，血红蛋白释放引起的溶血，比色法形成乳酸来估计细胞膜的扰动和使用荧光抗体的神经酰胺。苯并鎓（= 5µM）暴露48小时显着增加了胞质Ca 2 + 的浓度，降低了前向散射并触发了膜联蛋白V结合，在5 µM苯并鎓中影响了约30％的红细胞。经处理的红细胞中只有5％溶血。在名义上不存在Ca 2 + 和阿米洛利（1 mM）存在的情况下，苄索铵对膜联蛋白V结合的影响减弱了，而在全胰蛋白酶抑制剂zVAD（10 µM）的存在下则没有。苯并tho灵还显着增强了葡萄糖耗竭对胞质Ca 2 + 浓度和膜联蛋白V结合的影响，但显着减弱了葡萄糖耗竭对正向散射的影响。苯并tho（5 µM）显着增强了乳酸的形成，但并未增加神经酰胺的丰度。本观察结果揭示了苄索铵的新颖作用，即引发红细胞自杀死亡。

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