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

Molecular & Cellular Toxicology

Hana Lee¹  Woo-In Ryu¹  Yoon-Hee Park¹  Sang Hoon Jeong¹  Jin Hee Kim¹  Hyun Cheol Bae¹  Sang Wook Son¹ 

[1] Korea University College of Medicine$$

关键词: Nanoparticle;   

DOI  :  10.1007/s13273-014-0043-6

学科分类：分子生物学，细胞生物学和基因

来源: Korean Society of Toxicogenomics and Toxicoproteomics

【 摘 要 】

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.

【 授权许可】

Unknown