PUBLICATION

Protective effects of resveratrol against the cardiac developmental toxicity of trichloroethylene in zebrafish embryos

Authors
Huang, Y., Xia, Y., Tao, Y., Jin, H., Ji, C., Aniagu, S., Chen, T., Jiang, Y.
ID
ZDB-PUB-210202-23
Date
2021
Source
Toxicology   452: 152697 (Journal)
Registered Authors
Keywords
AHR, Heart development, Oxidative stress, Resveratrol, Trichloroethylene, Zebrafish
MeSH Terms
  • Animals
  • Cardiotonic Agents/pharmacology*
  • Embryonic Development/drug effects*
  • Embryonic Development/physiology
  • Heart/drug effects*
  • Heart/embryology*
  • Resveratrol/pharmacology*
  • Solvents/toxicity
  • Trichloroethylene/toxicity*
  • Zebrafish
PubMed
33524428 Full text @ Toxicology
CTD
33524428
Abstract
Trichloroethylene (TCE), a prevalent environmental contaminant, has been shown to induce cardiac malformations. Resveratrol (RSV) is a natural polyphenolic compound exhibiting protective effects on heart development. To investigate if RSV could protect against TCE-induced heart defects, we exposed zebrafish embryos to TCE (10 ppb) in the presence or absence of RSV (1 μg/mL). Our results showed that RSV significantly attenuated TCE-induced heart defects in zebrafish embryos. The TCE-induced ROS (reactive oxygen species) generation, 8-OHdG (8-hydroxy-2`-deoxyguanosine) formation and cell proliferation were significantly counteracted by RSV. Moreover, RSV attenuated the TCE-induced changes in mRNA expression or activity of genes involved in AHR and Nrf2 signal pathways. We further showed that RSV might inhibit TCE-enhanced cell proliferation by rescuing the downregulation of the p53/p21 axis. In conclusion, our data demonstrates that RSV protects against the cardiac developmental toxicity of TCE by inhibiting AHR activity, oxidative stress and cell proliferation.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping