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首页> 外文期刊>American Journal of Physiology >Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells: role of the plasma membrane Ca2+-ATPase.
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Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells: role of the plasma membrane Ca2+-ATPase.

机译：胰腺腺泡细胞中氧化剂受损的细胞内Ca2 +信号传导：质膜Ca2 + -ATPase的作用。

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Pancreatitis is an inflammatory disease of pancreatic acinar cells whereby intracellular calcium concentration ([Ca(2+)](i)) signaling and enzyme secretion are impaired. Increased oxidative stress has been suggested to mediate the associated cell injury. The present study tested the effects of the oxidant, hydrogen peroxide, on [Ca(2+)](i) signaling in rat pancreatic acinar cells by simultaneously imaging fura-2, to measure [Ca(2+)](i), and dichlorofluorescein, to measure oxidative stress. Millimolar concentrations of hydrogen peroxide increased cellular oxidative stress and irreversibly increased [Ca(2+)](i), which was sensitive to antioxidants and removal of external Ca(2+), and ultimately led to cell lysis. Responses were also abolished by pretreatment with (sarco)endoplasmic reticulum Ca(2+)-ATPase inhibitors, unless cells were prestimulated with cholecystokinin to promote mitochondrial Ca(2+) uptake. This suggests that hydrogen peroxide promotes Ca(2+) release from the endoplasmic reticulum and the mitochondria and that it promotes Ca(2+) influx. Lower concentrations of hydrogen peroxide (10-100 muM) increased [Ca(2+)](i) and altered cholecystokinin-evoked [Ca(2+)](i) oscillations with marked heterogeneity, the severity of which was directly related to oxidative stress, suggesting differences in cellular antioxidant capacity. These changes in [Ca(2+)](i) also upregulated the activity of the plasma membrane Ca(2+)-ATPase in a Ca(2+)-dependent manner, whereas higher concentrations (0.1-1 mM) inactivated the plasma membrane Ca(2+)-ATPase. This may be important in facilitating "Ca(2+) overload," resulting in cell injury associated with pancreatitis.
机译：胰腺炎是胰腺腺泡细胞的炎性疾病，因此细胞内钙浓度（[Ca（2 +）]（i））信号传导和酶分泌受到损害。已经建议增加氧化应激来介导相关的细胞损伤。本研究通过同时对fura-2成像以测量[Ca（2 +）]（i），测试了氧化剂双氧水对大鼠胰腺腺泡细胞中[Ca（2 +）]（i）信号的影响，和二氯荧光素，以测量氧化应激。毫摩尔浓度的过氧化氢增加了细胞的氧化应激，并且不可逆地增加了[Ca（2 +）]（i），这对抗氧化剂和外部Ca（2+）的去除很敏感，最终导致细胞溶解。响应也被（sarco）内质网Ca（2 +）-ATPase抑制剂取消，除非用胆囊收缩素预先刺激细胞以促进线粒体Ca（2+）摄取。这表明过氧化氢促进从内质网和线粒体释放Ca（2+），并促进Ca（2+）流入。较低浓度的过氧化氢（10-100μM）增加[Ca（2 +）]（i）并改变胆囊收缩素诱发的[Ca（2 +）]（i）振荡，具有明显的异质性，其严重程度与氧化应激，表明细胞抗氧化能力的差异。 [Ca（2 +）]（i）中的这些变化还以Ca（2+）依赖的方式上调了质膜Ca（2 +）-ATPase的活性，而更高的浓度（0.1-1 mM）灭活了质膜Ca（2 +）-ATPase。这可能对促进“ Ca（2+）超负荷”很重要，从而导致与胰腺炎相关的细胞损伤。

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