PUBLICATION

Molecular mechanisms of 2,3,7,8-tetrachlorodibenzo-p-dioxin cardiovascular embryotoxicity

Authors
Goldstone, H.M., and Stegeman, J.J.
ID
ZDB-PUB-060517-18
Date
2006
Source
Drug Metabolism Reviews   38(1-2): 261-289 (Review)
Registered Authors
Goldstone, Heather M. H., Stegeman, John J.
Keywords
none
MeSH Terms
  • Cardiovascular Abnormalities/chemically induced*
  • Cardiovascular Abnormalities/pathology
  • Structure-Activity Relationship
  • Animals
  • Reactive Oxygen Species/metabolism
  • Vascular Endothelial Growth Factor A/metabolism
  • Humans
  • Toxicogenetics
  • Embryo, Mammalian/physiology
  • Teratogens/chemistry
  • Teratogens/toxicity*
  • Receptors, Aryl Hydrocarbon/drug effects
PubMed
16684661 Full text @ Drug Metab. Rev.
Abstract
2,3,7,8 Tetrachlorodibenzo-p-dioxin (TCDD) and related planar halogenated aromatic hydrocarbons are widespread environmental contaminants and potent developmental toxicants. Hallmarks of embryonic exposure include edema, hemorrhage, and mortality. Recent studies in zebrafish and chicken have revealed direct impairment of cardiac muscle growth that may underlie these overt symptoms. TCDD toxicity is mediated by the aryl hydrocarbon receptor, but downstream targets remain unclear. Oxidative stress and growth factor modulation have been implicated in TCDD cardiovascular toxicity. Gene expression profiling is elucidating additional pathways by which TCDD might act. We review our understanding of the mechanism of TCDD embryotoxicity at morphological and molecular levels.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping