Ahmad Javed, Alhadlaq Hisham A, Alshamsan Aws, Siddiqui Maqsood A, Saquib Quaiser, Khan Shams T, Wahab Rizwan, Al-Khedhairy Abdulaziz A, Musarrat Javed, Akhtar Mohd Javed, Ahamed Maqusood
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Al-Jeraisy Chair for DNA Research, King Saud University, Riyadh, Saudi Arabia.
J Appl Toxicol. 2016 Oct;36(10):1284-93. doi: 10.1002/jat.3299. Epub 2016 Feb 25.
Copper ferrite nanoparticles (NPs) have the potential to be applied in biomedical fields such as cell labeling and hyperthermia. However, there is a lack of information concerning the toxicity of copper ferrite NPs. We explored the cytotoxic potential of copper ferrite NPs in human lung (A549) and liver (HepG2) cells. Copper ferrite NPs were crystalline and almost spherically shaped with an average diameter of 35 nm. Copper ferrite NPs induced dose-dependent cytotoxicity in both types of cells, evident by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide and neutral red uptake assays. However, we observed a quite different susceptibility in the two kinds of cells regarding toxicity of copper ferrite NPs. Particularly, A549 cells showed higher susceptibility against copper ferrite NP exposure than those of HepG2 cells. Loss of mitochondrial membrane potential due to copper ferrite NP exposure was observed. The mRNA level as well as activity of caspase-3 enzyme was higher in cells exposed to copper ferrite NPs. Cellular redox status was disturbed as indicated by induction of reactive oxygen species (oxidant) generation and depletion of the glutathione (antioxidant) level. Moreover, cytotoxicity induced by copper ferrite NPs was efficiently prevented by N-acetylcysteine treatment, which suggests that reactive oxygen species generation might be one of the possible mechanisms of cytotoxicity caused by copper ferrite NPs. To the best of our knowledge, this is the first report showing the cytotoxic potential of copper ferrite NPs in human cells. This study warrants further investigation to explore the mechanisms of differential toxicity of copper ferrite NPs in different types of cells. Copyright © 2016 John Wiley & Sons, Ltd.
铜铁氧体纳米颗粒（NPs）有潜力应用于细胞标记和热疗等生物医学领域。然而，关于铜铁氧体NPs的毒性信息却很匮乏。我们探究了铜铁氧体NPs对人肺（A549）细胞和肝（HepG2）细胞的细胞毒性潜力。铜铁氧体NPs呈晶体状，几乎为球形，平均直径为35纳米。通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐和中性红摄取试验可知，铜铁氧体NPs在这两种细胞中均诱导了剂量依赖性细胞毒性。然而，我们观察到这两种细胞对铜铁氧体NPs毒性的敏感性差异很大。特别是，A549细胞比HepG2细胞对铜铁氧体NP暴露表现出更高的敏感性。观察到由于铜铁氧体NP暴露导致线粒体膜电位丧失。在暴露于铜铁氧体NPs的细胞中，caspase-3酶的mRNA水平和活性更高。细胞氧化还原状态受到干扰，表现为活性氧（氧化剂）生成增加和谷胱甘肽（抗氧化剂）水平降低。此外，N-乙酰半胱氨酸处理有效地预防了铜铁氧体NPs诱导的细胞毒性，这表明活性氧生成可能是铜铁氧体NPs引起细胞毒性的可能机制之一。据我们所知，这是第一份显示铜铁氧体NPs在人类细胞中的细胞毒性潜力的报告。本研究值得进一步调查，以探索铜铁氧体NPs在不同类型细胞中差异毒性的机制。版权所有© 2016约翰威立父子有限公司。
