PUBLICATION

Induction of oxidative stress and apoptosis by silver nanoparticles in the liver of adult zebrafish

Authors
Choi, J.E., Kim, S., Ahn, J.H., Youn, P., Kang, J.S., Park, K., Yi, J., and Ryu, D.Y.
ID
ZDB-PUB-100112-26
Date
2010
Source
Aquatic toxicology (Amsterdam, Netherlands)   100(2): 151-159 (Journal)
Registered Authors
Keywords
Ag, Nanoparticle, Zebrafish, Liver, Oxidative stress, Apoptosis.
MeSH Terms
  • Animals
  • Apoptosis
  • Catalase/genetics
  • Catalase/metabolism
  • Glutathione/metabolism
  • Glutathione Peroxidase/genetics
  • Glutathione Peroxidase/metabolism
  • Liver/drug effects*
  • Liver/metabolism
  • Liver/ultrastructure
  • Malondialdehyde/metabolism
  • Metal Nanoparticles/toxicity*
  • Metal Nanoparticles/ultrastructure
  • Metallothionein/genetics
  • Metallothionein/metabolism
  • Oxidative Stress
  • Silver/metabolism
  • Silver/toxicity*
  • Superoxide Dismutase/genetics
  • Superoxide Dismutase/metabolism
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/physiology*
PubMed
20060176 Full text @ Aquat. Toxicol.
Abstract
Silver nanoparticles (AgNPs) may induce deleterious effects in aquatic life on environmental release. The hepatotoxicity of AgNPs was assessed in the liver of adult zebrafish, with the aim of studying the roles of oxidative damage and apoptosis. Zebrafish were exposed to an AgNP solution in which free Ag(+) ions were absent at the time of treatment. However, the metal-sensitive metallothionein 2 (MT2) mRNA was induced in the liver tissues of AgNP-treated zebrafish, suggesting that Ag(+) ions were released from AgNPs after treatment. It is also possible that MT2 mRNA was induced in the liver tissues by AgNP-generated free radicals. A number of cellular alterations including disruption of hepatic cell cords and apoptotic changes were observed in histological analysis of the liver tissues. The levels of malondialdehyde, a byproduct of cellular lipid peroxidation, and total glutathione were increased in the tissues after treatment with AgNPs. The mRNA levels of the oxyradical-scavenging enzymes catalase and glutathione peroxidase 1a were reduced in the tissues. AgNP treatment induced DNA damage, as demonstrated by analysis with the double-strand break marker gamma-H2AX and the expression of p53 protein in liver tissues. In addition, the p53-related pro-apoptotic genes Bax, Noxa, and p21 were upregulated after treatment with AgNPs. These data suggest that oxidative stress and apoptosis are associated with AgNP toxicity in the liver of adult zebrafish.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping