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首页> 外文期刊>Cellular Physiology and Biochemistry >Trifluoperazine-Induced Suicidal Erythrocyte Death and S-Nitrosylation Inhibition, Reversed by the Nitric Oxide Donor Sodium Nitroprusside
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Trifluoperazine-Induced Suicidal Erythrocyte Death and S-Nitrosylation Inhibition, Reversed by the Nitric Oxide Donor Sodium Nitroprusside

机译：三氟拉嗪诱导的自杀性红细胞死亡和S-亚硝基化抑制作用，被一氧化氮供体硝普钠逆转

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>Background and Purpose: The high potency antipsychotic drug trifluoperazine (10-[3-(4-methyl-1-piperazinyl)-propyl]-2-(trifluoromethyl)-(10)H-phenothiazine dihydrochloride; TFP) may either counteract or promote suicidal cell death or apoptosis. Similar to apoptosis, erythrocytes may enter eryptosis, characterized by phosphatidylserine exposure at the cell surface and cell shrinkage. Eryptosis can be stimulated by an increase in cytoplasmic Ca2+ concentration ([Ca2+]i) and inhibited by nitric oxide (NO). We explored whether TFP treatment of erythrocytes induces phosphatidylserine exposure, cell shrinkage, and calcium influx, whether it impairs S-nitrosylation and whether these effects are inhibited by NO. Methods: Phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, and protein nitrosylation from fluorescence switch of the Bodipy-TMR/Sypro Ruby signal. Results: Exposure of human erythrocytes to TFP significantly enhanced the percentage of annexin-V-binding cells, raised [Ca2+]i, and decreased S-nitrosylation. The effect of TFP on annexin-V-binding was not affected by removal of extracellular Ca2+ alone, but was significantly inhibited by pre-treatment with sodium nitroprusside (SNP), an effect significantly augmented by additional removal of extracellular Ca2+. A 3 hours treatment with 0.1 ?μM Ca2+ ionophore ionomycin triggered annexin-V-binding and cell shrinkage, effects fully reversed by removal of extracellular Ca2+. Conclusions: TFP induces eryptosis and decreases protein S-nitrosylation, effects blunted by nitroprusside. The effect of nitroprusside is attenuated in the presence of extracellular Ca2+.
机译：> 背景和目的： 高效抗精神病药物三氟拉嗪（10- [3-（4-甲基-1-哌嗪基）-丙基] -2-（三氟甲基）-（10）H-吩噻嗪盐酸盐（TFP）可能抵消或促进自杀细胞死亡或凋亡。与细胞凋亡相似，红细胞可能进入加密状态，其特征是磷脂酰丝氨酸暴露于细胞表面和细胞收缩。胞浆中Ca 2 + 浓度（[Ca 2 + ] i ）的增加可刺激加密，而一氧化氮（NO）则可抑制。我们探讨了TFP处理红细胞是否会诱导磷脂酰丝氨酸暴露，细胞收缩和钙流入，是否损害S-亚硝基化以及这些作用是否被NO抑制。 方法： 细胞膜上磷脂酰丝氨酸的暴露是根据膜联蛋白-V-结合，前向散射和[Ca 2 + ] <来自Fluo3-荧光的sub> i 和来自Bodipy-TMR / Sypro Ruby信号的荧光开关的蛋白质亚硝基化。 结果： 人类红细胞暴露于TFP显着增强了膜联蛋白-V结合细胞的百分比，提高了[Ca 2 + ] i ，并减少S-亚硝基化。 TFP对膜联蛋白-V结合的作用不受单独去除细胞外Ca 2 + 的影响，但通过硝普钠（SNP）的预处理可显着抑制，而额外添加去除细胞外Ca 2 + 。用0.1？​​μMCa 2 + 离子载体离子霉素处理3小时会触发膜联蛋白-V结合和细胞收缩，通过去除细胞外Ca 2 + 可以完全逆转作用。 结论： TFP可以诱导加密并减少蛋白质S-亚硝基化，而硝普钠的作用减弱了。在细胞外Ca 2 + 存在下，硝普钠的作用减弱。

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