Human exposure to manufactured nanoparticles (NPs) is a public health concern. Endothelial cells lining the inner surface of arteries could be one of the primary targets for inhaled nanoparticles. Moreover, it is well known that alteration in calcium signaling is a critical event involved in the physiopathology of cardiovascular diseases. The objective of this study was to assess the role of oxidative stress in carbon black FW2 NPs-induced alteration in calcium signaling and mitochondria in human pulmonary artery endothelial cells. To this end, cells were exposed for 4 or 24 h to FW2 NPs (1-10 μg/cm2) and the following endpoints were studied: (i) production of ROS by fluorimetry and electron paramagnetic resonance, (ii) variation in intracellular calcium concentration by confocal microscopy, and (iii) mitochondrial alteration and apoptosis by confocal microscopy and transmission electronic microscopy. Exposure to FW2 NPs concentration-dependently increases oxidative stress, evidenced by the production of superoxide anion leading to an alteration in calcium content of intracellular organelles, such as endoplasmic reticulum and mitochondria activating, in turn, intrinsic apoptosis. This study provides evidence that FW2 NPs exposure impairs calcium signaling and mitochondria triggered by oxidative stress, and, thus, could act as a cardiovascular disease risk owing to the key role of calcium homeostasis in the control of vascular tone.

中文翻译：

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炭黑纳米粒子对人肺动脉内皮细胞的体外研究：对钙信号和线粒体变化的影响。

人体暴露于人造纳米颗粒（NPs）是一个公共健康问题。衬在动脉内表面的内皮细胞可能是吸入纳米颗粒的主要靶标之一。而且，众所周知，钙信号传导的改变是涉及心血管疾病的生理病理学的关键事件。这项研究的目的是评估氧化应激在炭黑FW2 NPs诱导的人肺动脉内皮细胞钙信号传导和线粒体改变中的作用。为此，将细胞暴露于FW2 NP（1-10μg/ cm2）4或24 h，并研究了以下终点：（i）通过荧光法和电子顺磁共振产生ROS，（ii）细胞内钙的变化共聚焦显微镜浓缩 （iii）通过共聚焦显微镜和透射电子显微镜观察线粒体的改变和凋亡。暴露于FW2 NPs浓度依赖性地增加氧化应激，这由超氧化物阴离子的产生所证明，导致细胞内细胞器（例如内质网和线粒体）钙含量的改变，进而激活内在凋亡。这项研究提供的证据表明，FW2 NPs的暴露会损害由氧化应激触发的钙信号传导和线粒体，因此，由于钙稳态在控制血管紧张中的关键作用，因此可能成为心血管疾病的风险。由超氧化物阴离子的产生所证实，该超氧化物阴离子导致细胞内细胞器（例如内质网和线粒体）的钙含量改变，进而激活内在凋亡。这项研究提供的证据表明，FW2 NPs的暴露会损害由氧化应激触发的钙信号传导和线粒体，因此，由于钙稳态在控制血管紧张中的关键作用，因此可能成为心血管疾病的风险。由超氧化物阴离子的产生所证实，该超氧化物阴离子导致细胞内细胞器（例如内质网和线粒体）的钙含量改变，进而激活内在凋亡。这项研究提供的证据表明，FW2 NPs的暴露会损害由氧化应激触发的钙信号传导和线粒体，因此，由于钙稳态在控制血管紧张中的关键作用，因此可能成为心血管疾病的风险。