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Zinc oxide nanoparticle induced autophagic cell death and mitochondrial damage via reactive oxygen species generation

Cited 165 time in Web of Science Cited 164 time in Scopus
Authors
Yu, Kyeong-Nam; Yoon, Tae-Jong; Minai-Tehrani, Arash; Kim, Ji-Eun; Park, Soo Jin; Jeong, Min Sook; Ha, Shin-Woo; Lee, Jin-Kyu; Kim, Jun Sung; Cho, Myung-Haing
Issue Date
2013-06
Citation
Toxicology in Vitro, Vol.27 No.4, pp.1187-1195
Keywords
Zinc oxide nanoparticlesCytotoxicityAutophagyReactive oxygen species (ROS)Mitochondria damage
Abstract
Zinc oxide nanoparticles (ZnO-np) are used in an increasing number of industrial products such as paint, coating and cosmetics, and in other biological applications. There have been many suggestions of a ZnO-np toxicity paradigm but the underlying molecular mechanisms about the toxicity of ZnO-np remain unclear. This study was done to determine the potential toxicity of ZnO-np and to assess the toxicity mechanism in normal skin cells. Synthesized ZnO-np generated reactive oxygen species (ROS), as determined by electron spin resonance. After uptake into cells, ZnO-np induced ROS in a concentration- and time-dependent manner. To demonstrate ZnO-np toxicity mechanism related to ROS, we detected abnormal autophagic vacuoles accumulation and mitochondria dysfunction after ZnO-np treatment. Furthermore mitochondria membrane potential and adenosine-5'-triphosphate (ATP) production are decreased for culture with ZnO-np. We conclude that ZnO-np leads to cell death through autophagic vacuole accumulation and mitochondria damage in normal skin cells via ROS induction. Accordingly, ZnO-np may cause toxicity and the results highlight and need for careful regulation of ZnO-np production and use. (C) 2013 Elsevier Ltd. All rights reserved.
ISSN
0887-2333
URI
https://hdl.handle.net/10371/172524
DOI
https://doi.org/10.1016/j.tiv.2013.02.010
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College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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