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首页> 外文期刊>Archives of Toxicology >Effect of calmidazolium on [Ca2+]i and viability in human hepatoma cells
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Effect of calmidazolium on [Ca2+]i and viability in human hepatoma cells

机译：甲硝唑对人肝癌细胞中[Ca 2 + ] i 的影响

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The effect of calmidazolium on cytosolic free Ca2+ concentrations ([Ca2+]i) and viability has not been explored in human hepatoma cells. This study examined whether calmidazolium altered [Ca2+]i and caused cell death in HA59T cells. [Ca2+]i and cell viability were measured using the fluorescent dyes fura-2 and WST-1, respectively. Calmidazolium at concentrations ≥1 μM increased [Ca2+]i in a concentration-dependent manner with an EC50 value of 1.5 μM. The Ca2+ signal was reduced partly by removing extracellular Ca2+. Calmidazolium induced Mn2+ quench of fura-2 fluorescence implicating Ca2+ influx. The Ca2+ influx was insensitive to L-type Ca2+ entry blockers, but was inhibited partly by enhancing or inhibiting protein kinase C activity. In Ca2+-free medium, after pretreatment with 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), calmidazolium-induced [Ca2+]i rises were largely inhibited; and conversely, calmidazolium pretreatment totally suppressed thapsigargin-induced [Ca2+]i rises. Inhibition of phospholipase C with 2 μM U73122 did not change calmidazolium-induced [Ca2+]i rises. At concentrations between 1 and 15 μM, calmidazolium induced apoptosis-mediated cell death. Collectively, in HA59T hepatoma cells, calmidazolium induced [Ca2+]i rises by causing Ca2+ release from the endoplasmic reticulum in a phospholipase C-independent manner, and Ca2+ influx via protein kinase C-regulated Ca2+ entry pathway. Calmidazolium caused cytotoxicity via apoptosis.
机译：在人肝癌细胞中尚未探讨卡地咪唑对胞质游离Ca 2 + 浓度（[Ca 2 + ] i ）和活力的影响。 。这项研究检查了卡地咪唑是否改变了HA59T细胞中的[Ca 2 + ] i 并引起了细胞死亡。使用荧光染料fura-2和WST-1分别测量[Ca 2 + ] i 和细胞活力。浓度≥1μM的咪唑鎓以浓度依赖的方式增加[Ca 2 + ] i ，EC 50 值为1.5μM。通过去除细胞外Ca 2 + ，部分减少了Ca 2 + 信号。钙咪唑诱导呋喃2荧光的Mn 2 + 猝灭，提示Ca 2 + 大量涌入。 Ca 2 + 涌入对L型Ca 2 + 进入阻滞剂不敏感，但部分被增强或抑制蛋白激酶C活性所抑制。在不含Ca 2 + 的培养基中，用1μMthapsigargin（内质网Ca 2 + 泵抑制剂）预处理后，由卡地咪唑诱导的[Ca 2+ < / sup>] i 的上升在很大程度上受到抑制；相反，卡介唑预处理可以完全抑制thapsigargin诱导的[Ca 2 + ] i 的升高。用2μMU73122抑制磷脂酶C不会改变卡尼地唑诱导的[Ca 2 + ] i 升高。在1至15μM的浓度下，卡地咪唑诱导凋亡介导的细胞死亡。总体上，在HA59T肝癌细胞中，卡介唑诱导的Ca 2 + 从磷脂酶从内质网释放，诱导[Ca 2 + ] i 升高C依赖性方式，并且Ca 2 + 通过蛋白激酶C调节Ca 2 + 进入途径流入。咪唑鎓通过细胞凋亡引起细胞毒性。

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