Nickel oxide nanoparticles induce inflammation and genotoxic effect in lung epithelial cells

被引:122
|
作者
Capasso, Laura [1 ]
Camatini, Marina [1 ]
Gualtieri, Maurizio [1 ]
机构
[1] Univ Milano Bicocca, Polaris Res Ctr, I-20126 Milan, Italy
关键词
Interleukins; MAP-kinases; NF-kB; Nickel oxide nanoparticles; Pulmonary epithelial cells; ROS; TITANIUM-DIOXIDE NANOPARTICLES; OXIDATIVE STRESS; A549; CELLS; INTRATRACHEAL INSTILLATION; SILVER NANOPARTICLES; METALLIC NICKEL; BEAS-2B CELLS; DNA-DAMAGE; ACTIVATION; APOPTOSIS;
D O I
10.1016/j.toxlet.2014.01.040
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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.
引用
收藏
页码:28 / 34
页数:7
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