PUBLICATION

Indium and Indium Tin Oxide Induce Endoplasmic Reticulum Stress and Oxidative Stress in Zebrafish (Danio rerio)

Authors
Brun, N.R., Christen, V., Furrer, G., Fent, K.
ID
ZDB-PUB-140905-1
Date
2014
Source
Environmental science & technology   48(19): 11679-87 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Apoptosis
  • Endoplasmic Reticulum Stress*
  • Heat-Shock Proteins/chemistry
  • Indium/chemistry*
  • Inflammation
  • Liver/drug effects
  • Nitrates/chemistry*
  • Oxidative Stress/drug effects*
  • Reactive Oxygen Species/metabolism
  • Solubility
  • Tin Compounds/chemistry*
  • Tumor Necrosis Factor-alpha/metabolism
  • Zebrafish/metabolism*
PubMed
25188630 Full text @ Env. Sci. Tech.
Abstract
Indium and indium tin oxide (ITO) are extensively used in electronic technologies. They may be introduced into the environment during production, use, and leaching from electronic devices at the end of their life. At present, surprisingly little is known about potential ecotoxicological implications of indium contamination. Here, molecular effects of indium nitrate (In(NO3)3) and ITO nanoparticles were investigated in vitro in ZFL cells and in zebrafish embryos and provide novel insights into their molecular effects. In(NO3)3 led to induction of endoplasmic reticulum (ER) stress response, induction of reactive oxygen species (ROS) and induction of transcripts of pro-apoptotic genes and TNF-α in vitro. In(NO3)3 induced the ER stress key gene BiP at mRNA and protein level, as well as atf6 which ultimately led to induction of the important pro-apoptotic marker gene chop. The activity of In(NO3)3 on ER stress induction was much stronger than that of ITO, which is explained by differences in soluble free indium ion concentrations. The effect was also stronger in ZFL cells than in zebrafish embryos. Our study provides first evidence of ER stress and oxidative stress induction by In(NO3)3 and ITO indicating a critical toxicological profile that needs further investigation.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping