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

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• 作者：Woo-In Ryu (1)
  Yoon-Hee Park (1)
  Hyun Cheol Bae (1)
  Jin Hee Kim (1)
  Sang Hoon Jeong (1)
  Hana Lee (1)
  Sang Wook Son (1)
  
  1. Laboratory of Cell Signaling and Nanomedicine ; Department of Dermatology ; Division of Brain Korea 21 Project for Biomedical Science ; Korea University College of Medicine ; Seoul ; Korea
  
• 关键词：Zinc Oxide ; Cytotoxicity ; Reactive oxygen species ; Keratinocyte ; Nanoparticle
• 刊名：Molecular & Cellular Toxicology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：10
• 期：4
• 页码：387-391
• 全文大小：341 KB
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• 刊物主题：Cell Biology; Pharmacology/Toxicology;
• 出版者：Springer Netherlands
• ISSN：2092-8467

文摘

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.