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Cytotoxicity, oxidative stress, and genotoxicity in human hepatocyte and embryonic kidney cells exposed to ZnO nanoparticles

Rongfa Guan1*, Tianshu Kang1, Fei Lu2, Zhiguo Zhang3, Haitao Shen4 and Mingqi Liu1

  • * Corresponding author: Rongfa Guan rfguan@163.com

  • † Equal contributors

Author Affiliations

1 Zhejiang Provincial Key Laboratory of Biometrology and Inspection and Quarantine, China Jiliang University, Hangzhou 310018, People's Republic of China

2 College of Biological and Environmental Engineering, Zhejiang University of Technology, Hangzhou, 310014, People's Republic of China

3 Food Science Institute, Zhejiang Academy of Agricultural Sciences, Hangzhou, 310021, People's Republic of China

4 Zhejiang Province Center for Disease Prevention and Control (ZJCDC), HangZhou, 310051, People's Republic of China

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Nanoscale Research Letters 2012, 7:602  doi:10.1186/1556-276X-7-602

Published: 30 October 2012

Abstract

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.

Keywords:
ZnO nanoparticles; Cytotoxicity; Oxidative stress; Human hepatocyte; Human embryonic kidney cells