PUBLICATION

Determination and prediction of the binding interaction between organophosphate flame retardants and p53

Authors
Li, F., Yang, X., Li, X., Li, R., Zhao, J., Wu, H.
ID
ZDB-PUB-170214-279
Date
2014
Source
Chemical Research in Toxicology   27: 1918-25 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Tumor Suppressor Protein p53/genetics
  • Tumor Suppressor Protein p53/metabolism*
  • Cell Line
  • Flame Retardants/metabolism*
  • Flame Retardants/toxicity
  • Quantitative Structure-Activity Relationship
  • Environmental Pollutants/chemistry
  • Environmental Pollutants/metabolism*
  • Environmental Pollutants/toxicity
  • Kinetics
  • Organophosphates/chemistry
  • Organophosphates/metabolism*
  • Organophosphates/toxicity
  • Protein Binding
  • Molecular Dynamics Simulation
  • Zebrafish
  • Molecular Docking Simulation
  • Fibroblasts/drug effects
  • Fibroblasts/metabolism
  • Hydrogen Bonding
  • Animals
PubMed
25333763 Full text @ Chem. Res. Toxicol.
CTD
25333763
Abstract
Organophosphate flame retardants (OPFRs) have caused widespread concern because of the harm to the environment. In this study, to better explain the mechanism for the binding of OPFRs with the tumor suppressor gene p53, an integrated experimental and in silico approach was used. The binding constants of 10 OPFRs were measured by surface plasmon resonance technology (SPR). The effect of OPFRs on p53 gene and protein expression in ZF4 cells was determined by quantitative real-time PCR and Western blotting. Molecular docking and dynamics simulation were explored to find that the H-bonds and hydrophobic interactions were the dominant interaction between OPFRs and p53. On the basis of the observed interactions, proper molecular structural descriptors were used to build the quantitative structure-activity relationship (QSAR) model. The current QSAR model provided robustness, predictive ability, and mechanism interpretability. The applicability domain of the QSAR was discussed by the Williams plot. The results showed that H-bonds and electrostatic interaction governed the binding affinities between OPFRs and p53.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping