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氧化锌纳米颗粒诱导人肝细胞(HepG2)氧化应激和遗传毒性。

Zinc oxide nanoparticles induce oxidative stress and genotoxicity in human liver cells (HepG2).

机构信息

Nanomaterial Toxicology Group, Indian Institute of Toxicology Research (CSIR), P.O. Box 80, M. G. Marg, Lucknow 226001, India.

出版信息

J Biomed Nanotechnol. 2011 Feb;7(1):98-9. doi: 10.1166/jbn.2011.1220.

Abstract

Zinc oxide (ZnO) is being used worldwide in consumer products and industrial applications. As humans are being directly exposed to ZnO nanoparticles (NPs) through different routes, it is likely that the NPs would gain access to the liver. Therefore, the present study investigated the cytotoxic and genotoxic potential of ZnO nanoparticles in human liver cells (HepG2). The MTT and neutral red uptake assay showed a significant (p < 0.05) concentration and time dependent toxicity after 12 and 24 h at 14 and 20 microg/ml. A (p < 0.05) significant increase in DNA damage was observed in cells exposed to ZnO NPs for 6 h as evident with an increase in the Olive tail moment (OTM) and % tail DNA in the Comet assay. The generation of intracellular reactive oxygen species further suggest the role of oxidative stress in ZnO nanoparticle mediated DNA damage and cytotoxicity in HepG2 cells.

摘要

氧化锌 (ZnO) 正被广泛应用于消费产品和工业应用中。由于人类通过不同途径直接接触氧化锌纳米粒子 (NPs),因此 NPs 很可能进入肝脏。因此,本研究调查了 ZnO 纳米粒子在人肝细胞 (HepG2) 中的细胞毒性和遗传毒性。MTT 和中性红摄取试验显示,在 14 和 20 μg/ml 时,12 和 24 h 后,浓度和时间依赖性毒性显著 (p < 0.05)。彗星试验显示,细胞暴露于 ZnO NPs 6 h 后,DNA 损伤明显增加,Olive 尾部矩 (OTM) 和尾巴 DNA 的百分比增加。细胞内活性氧的产生进一步表明氧化应激在 ZnO 纳米颗粒介导的 HepG2 细胞 DNA 损伤和细胞毒性中的作用。

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