Nickel oxide nanoparticles induce inflammation and genotoxic effect in lung epithelial cells
Nickel oxide nanoparticles induce inflammation and genotoxic effect in lung epithelial cells
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DOI：
10.1016/j.toxlet.2014.01.040
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发表时间：
2014-04-07
影响因子：
3.5
通讯作者：
Gualtieri, Maurizio
中科院分区：
文献类型：
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作者：
Capasso, Laura;Camatini, Marina;Gualtieri, Maurizio
已经在人肺上皮细胞系BEAS-2B和A549中评估了氧化镍纳米颗粒（NiONP）的毒性。以20、40、60、80、100 μ g/ml的剂量使用的纳米颗粒在24 h时诱导细胞活力的显著降低以及凋亡和坏死细胞的增加。在处理24小时后评估白细胞介素-6和-8的显著释放，甚至细胞内ROS在暴露后45分钟已经增加。结果表明，细胞因子的释放依赖于丝裂原活化蛋白激酶（MAPK）级联反应，通过NF-κ B途径的诱导。NiONP在两种细胞系中诱导细胞周期改变，即使在不同的阶段，这些修饰可能是由NP的遗传毒性效应诱导的，这由磷酸-ATM和磷酸-ATR的核转位提出。我们的研究结果证实了NiONP的细胞毒性和促炎潜力。此外，它们诱导DNA损伤反应的能力已被证明。这种作用存在于内化NP的A549细胞和未观察到内吞作用的BEAS-2B细胞中。(C)2014爱思唯尔爱尔兰有限公司版权所有。
Nickel oxide nanoparticles (NiONPs) toxicity has been evaluated in the human pulmonary epithelial cell lines: BEAS-2B and A549. The nanoparticles, used at the doses of 20, 40, 60, 80, 100 mu g/ml, induced a significant reduction of cell viability and an increase of apoptotic and necrotic cells at 24 h. A significant release of interleukin-6 and -8 was assessed after 24h of treatment, even intracellular ROS increased already at 45 min after exposure. The results obtained evidenced that the cytokines release was dependent on mitogen activated protein kinases (MAPK) cascade through the induction of NF-kB pathway. NiONPs induced cell cycle alteration in both the cell lines even in different phases and these modifications may be induced by the NPs genotoxic effect, suggested by the nuclear translocation of phospho-ATM and phospho-ATR. Our results confirm the cytotoxic and pro-inflammatory potential of NiONPs. Moreover their ability in inducing DNA damage responses has been demonstrated. Such effects were present in A549 cells which internalize the NPs and BEAS-2B cells in which endocytosis has not been observed. (C) 2014 Elsevier Ireland Ltd. All rights reserved.