ZnO nanoparticle induces apoptosis by ROS triggered mitochondrial pathway in human keratinocytes

Woo In Ryu, Yoon Hee Park, Hyun Cheol Bae, Jin Hee Kim, Sang Hoon Jeong, Hana Lee, Sang Wook Son

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


Zinc Oxide nanoparticles (ZnO NPs) in its small size with large reactive surfaces can lead to toxicological injury by generating reactive oxygen species (ROS) and oxidative stress. Recently, ZnO NPs were shown to play a role in acute or chronic toxicities with mammalian cells, where its mechanism of toxicity is not fully characterized yet. In this study, the potential mechanisms of ZnO NPs in inducing and increasing oxidative stress for causing cellular apoptosis were investigated with human keratinocytes. Indeed, ZnO NPs induced significant intracellular ROS and mitochondrial ROS productions. And it seemed that cellular ROS levels induced by ZnO NPs led to the dissipation of the mitochondrial membrane potentials and elicited the cellular apoptosis. The induced ROS production by ZnO NPs was blocked with chelator treatment, which inhibited the ZnO ion. The present study demonstrates that increased levels of ROS by ZnO NPs cause mitochondrial dysfunction and cellular apoptosis.

Original languageEnglish
Pages (from-to)387-391
Number of pages5
JournalMolecular and Cellular Toxicology
Issue number4
Publication statusPublished - 2014 Dec

Bibliographical note

Publisher Copyright:
© 2014, The Korean Society of Toxicogenomics and Toxicoproteomics and Springer Science+Business Media Dordrecht.


  • Cytotoxicity
  • Keratinocyte
  • Nanoparticle
  • Reactive oxygen species
  • Zinc Oxide

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Toxicology
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis


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