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首页> 外文期刊>Journal of biochemical and molecular toxicology >The cytosolic calcium concentration is affected by S-nitrosocysteine in human lymphomonocytes.
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The cytosolic calcium concentration is affected by S-nitrosocysteine in human lymphomonocytes.

机译：人淋巴单核细胞中的胞质钙浓度受S-亚硝基半胱氨酸的影响。

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摘要

The homeostasis of cytosolic calcium [Ca2+](c) in mammalian cells is a complex phenomenon, requiring the contribution of many cellular and extracellular systems. Nitric oxide (NO) acts on [Ca2+](c), although the mechanism of this action is unknown. We study the release and the uptake of Ca2+ in the endoplasmic reticulum and its capacitative entry in human lymphomonocytes in the presence of the NO donor S-nitrosocysteine (CysNO) at low (16 microM) and at high (160 microM) concentrations by measuring the [Ca2+](c) by the Fura 2-AM method. Thapsigargin (TG), which inhibits sarco-endoplasmic reticulum Ca2+-ATPase (SERCA), and nifedipine (NIF), which blocks the Ca2+ release from intracellular stores, are used to clarify the effects of NO on calcium movements. In the absence of extracellular Ca2+, CysNO decreases basal [Ca2+](c), whereas TG increases it as the result of SERCA inhibition. This effect of TG diminishes in the presence of the NO donor. In the presence of extracellular Ca2+(capacitative entry conditions), CysNO does not influence Ca2+ entry but reduces the toxic effects of TG connected to the increase of [Ca2+](c) in these conditions. The effect of NIF is, up to a certain extent, similar to that of CysNO, although the mechanisms of action of the two agents do not seem related. We conclude that CysNO participates in [Ca2+](c) homeostasis by stimulating the movement of the ion from the cytosol to other compartments.
机译：哺乳动物细胞中胞质钙[Ca2 +]（c）的稳态是一个复杂的现象，需要许多细胞和细胞外系统的参与。一氧化氮（NO）作用于[Ca2 +]（c），尽管该作用的机理尚不清楚。我们通过测量低浓度（16 microM）和高浓度（160 microM）的NO供体S-亚硝基半胱氨酸（CysNO）的存在来研究内质网中Ca2 +的释放和摄取及其在人淋巴细胞中的电容性进入。通过Fura 2-AM方法测得[Ca2 +]（c）。 Thapsigargin（TG）可以抑制肌内膜网状Ca2 + -ATPase（SERCA），硝苯地平（NIF）可以阻止Ca2 +从细胞内存储中释放出来，用于阐明NO对钙运动的影响。在不存在细胞外Ca2 +的情况下，CysNO降低了基础[Ca2 +]（c），而TG由于SERCA抑制而使其升高。在NO供体的存在下，TG的这种作用减弱。在细胞外Ca2 +存在的情况下（电容性进入条件），CysNO不会影响Ca2 +进入，但会降低在这些条件下与[Ca2 +]（c）的增加有关的TG的毒性作用。 NIF的作用在一定程度上类似于CysNO，尽管这两种药物的作用机制似乎无关。我们得出结论，CysNO通过刺激离子从胞质溶胶向其他区室的运动而参与[Ca2 +]（c）稳态。

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