Cited by 268Nanoparticles: synthesis and applicationsAutophagy in Disease and TherapyHeavy Metal Exposure and Toxicity

Zinc Oxide Nanoparticle Induced Autophagic Cell Death and Mitochondrial Damage via Reactive Oxygen Species Generation

Yu, Kyeong-Nam, Yoon, Tae-Jong, Minai-Tehrani, Arash, Kim, Ji-Eun, Park, Soo Jin, Jeong, Min Sook, Ha, Shin-Woo, Lee, Jin-Kyu +2 more·2013·Toxicology in Vitro

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.

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Registry

Crossref · 10.1016/j.tiv.2013.02.010

Cites

42 of 42 references verified0 citation errors · 0 not checkable

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  • Zinc overload can contribute to increased cellular oxidative stress and senescence through mechanisms possibly related to organelle dysfunction.

    “On the other hand, Zn overload can contribute to augment cellular OS and senescence through different mechanisms not yet well-defined, but possibly related to organelles dysfunction [411,427,438].”
  • Zinc deficiency causes destabilization of membrane structure and increases oxidative stress.

    “In this respect, evidence showed that Zn deficiency causes destabilization of membrane structure and augments OS [424,425,426,427,428].”

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Authors
Yu, K.-N., Yoon, T.-J., Minai-Tehrani, A., Kim, J.-E., Park, S. J., Jeong, M. S., Ha, S.-W., Lee, J.-K., Kim, J. S., & Cho, M.-H.
Affiliations
  • Seoul National University (KR)
  • CHA University (KR)
  • Emory University (US)
Corresponding author
  • Kim, Jun Sung
  • Cho, Myung-Haing
Venue
Toxicology in Vitro
Publisher
Elsevier BV
Published
2013-06
Volume
27
Issue
4
Pages
1187-1195
ISSN
0887-2333 (ISSN-L)
OpenAlex
W1966626824
Cited by
268
References
43
Citations by year
2026: 8 · 2025: 14 · 2024: 15 · 2023: 16 · 2022: 17 · 2021: 20 · 2020: 28 · 2019: 31 · 2018: 26 · 2017: 16 · 2016: 26 · 2015: 25 · 2014: 21 · 2013: 5
FWCI
11.58
Type
journal article
Language
en
Open access
closed
Locations
  • Toxicology in Vitro (publishedVersion)
  • PubMed (publishedVersion)
  • Seoul National University Open Repository (Seoul National University) (submittedVersion)
Funders
  • Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University
  • National Research Foundation of Korea
  • Ministry of Education, Science and Technology (2009-0082737, 2010-0019991, 2011-0019175)
Topics
  • Physical Sciences › Materials Science › Materials Chemistry › Nanoparticles: synthesis and applications
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
Keywords
zinc oxide nanoparticles, nanoparticle toxicity, autophagic cell death, mitochondrial damage, mitochondrial dysfunction, reactive oxygen species, mitochondrial membrane potential, ATP production, skin cells, nanoparticle uptake
MeSH terms
Adenosine Triphosphate, Animals, Autophagy, Cell Line, Mitochondria, Zinc Oxide, Reactive Oxygen Species, Microscopy, Electron, Transmission, Mice, Membrane Potential, Mitochondrial, Metal Nanoparticles

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