Cytotoxicity, oxidative stress, and genotoxicity in human hepatocyte and embryonic kidney cells exposed to ZnO nanoparticles.
Cytotoxicity, oxidative stress, and genotoxicity in human hepatocyte and embryonic kidney cells exposed to ZnO nanoparticles.
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DOI：
10.1186/1556-276x-7-602
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发表时间：
2012-10-30
影响因子：
--
通讯作者：
Liu M
中科院分区：
文献类型：
--
作者：
Guan R;Kang T;Lu F;Zhang Z;Shen H;Liu M
在肝脏和肾脏中可能发现微量的氧化锌纳米颗粒(氧化锌纳米颗粒)。本研究的目的是确定使用氧化锌纳米颗粒的最佳活性测定方法，并评价其对人肝细胞(L02)和人胚胎肾(HEK293)细胞的毒性。结果表明，氧化锌纳米粒可导致细胞形态改变、线粒体功能障碍、超氧化物歧化酶(SOD)氧化损伤、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)等氧化应激标志物的氧化损伤。氧化锌纳米颗粒毒性的确切机制表明，氧化应激和脂质过氧化在氧化锌纳米颗粒引起的细胞膜破坏、DNA损伤和随后的细胞死亡中起着重要作用。我们的初步数据表明，氧化应激可能参与了氧化锌纳米颗粒的细胞毒性。
Traces of zinc oxide nanoparticles (ZnO NPs) used may be found in the liver and kidney. The aim of this study is to determine the optimal viability assay for using with ZnO NPs and to assess their toxicity to human hepatocyte (L02) and human embryonic kidney (HEK293) cells. Cellular morphology, mitochondrial function (MTT assay), and oxidative stress markers (malondialdehyde, glutathione (GSH) and superoxide dismutase (SOD)) were assessed under control and exposed to ZnO NPs conditions for 24 h. The results demonstrated that ZnO NPs lead to cellular morphological modifications, mitochondrial dysfunction, and cause reduction of SOD, depletion of GSH, and oxidative DNA damage. The exact mechanism behind ZnO NPs toxicity suggested that oxidative stress and lipid peroxidation played an important role in ZnO NPs-elicited cell membrane disruption, DNA damage, and subsequent cell death. Our preliminary data suggested that oxidative stress might contribute to ZnO NPs cytotoxicity.