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Zinc oxide nanoparticle induced autophagic cell death and mitochondrial damage via reactive oxygen species generation
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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“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].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [427]
In the citing paper
“In this respect, evidence showed that Zn deficiency causes destabilization of membrane structure and augments OS [424,425,426,427,428].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [427]
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Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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