PUBLICATION

Estimation of the Oxidative Stress and Molecular Damage Caused by 1-Butyl-3-Methylimidazolium Bromide Ionic Liquid in Zebrafish Livers

Authors
Dong, M., Liu, T., Wang, J., Wang, J., Zhu, L., Zhang, J.
ID
ZDB-PUB-151219-4
Date
2016
Source
Journal of biochemical and molecular toxicology   30(5): 232-8 (Journal)
Registered Authors
Keywords
HPLC, MDA, DNA Damage, ROS, SOD
MeSH Terms
  • Animals
  • Catalase/metabolism
  • Comet Assay
  • DNA Fragmentation/drug effects*
  • Female
  • Imidazoles/toxicity*
  • Lipid Peroxidation/drug effects
  • Liver/drug effects*
  • Liver/metabolism
  • Liver/pathology
  • Male
  • Malondialdehyde/metabolism
  • Oxidation-Reduction
  • Oxidative Stress/drug effects
  • Reactive Oxygen Species/metabolism
  • Superoxide Dismutase/metabolism
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/metabolism*
PubMed
26681321 Full text @ J. Biochem. Mol. Toxicol.
Abstract
The present study investigated the toxic effects of 1-butyl-3-methylimidazolium bromide ([C4 mim]Br) in zebrafish livers after exposure to 5-40 mg/L of [C4 mim]Br on days 7, 14, 21, and 28. The results showed that low levels of [C4 mim]Br exposure activated the superoxide dismutase (SOD) activity during early periods of exposure. However, high concentrations (20-40 mg/L) of [C4 mim]Br caused the inhibition of SOD, which, accordingly, led to excess reactive oxygen species and malondialdehyde. The present results indicate that [C4 mim]Br causes oxidative stress in the livers of both male and female zebrafish. Additionally, the DNA damage revealed that [C4 mim]Br has a genotoxic effect on zebrafish livers, even when the concentration of [C4 mim]Br is low (5 mg/L). The DNA damage was demonstrated by quantifying the DNA strand breakage.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping