PUBLICATION
Benzo[a]pyrene exposure influences the cardiac development and the expression of cardiovascular relative genes in zebrafish (Danio rerio) embryos
- Authors
- Huang, L., Wang, C., Zhang, Y., Li, J., Zhong, Y., Zhou, Y., Chen, Y., and Zuo, Z.
- ID
- ZDB-PUB-120110-20
- Date
- 2012
- Source
- Chemosphere 87(4): 369-375 (Journal)
- Registered Authors
- Keywords
- B(a)P, cardiac toxicity, embryonic development, gene regulatory networks, microarray, zebrafish
- MeSH Terms
-
- Animals
- Benzo(a)pyrene/toxicity*
- Cardiovascular System/drug effects
- Cardiovascular System/metabolism
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/metabolism
- Embryo, Nonmammalian/physiology
- Gene Expression/drug effects
- Gene Expression Regulation, Developmental/drug effects
- Heart/drug effects
- Heart/growth & development*
- Heart/physiopathology
- Heart Defects, Congenital/chemically induced
- Myocardium/metabolism
- Water Pollutants, Chemical/toxicity*
- Zebrafish/embryology*
- PubMed
- 22209252 Full text @ Chemosphere
- CTD
- 22209252
Citation
Huang, L., Wang, C., Zhang, Y., Li, J., Zhong, Y., Zhou, Y., Chen, Y., and Zuo, Z. (2012) Benzo[a]pyrene exposure influences the cardiac development and the expression of cardiovascular relative genes in zebrafish (Danio rerio) embryos. Chemosphere. 87(4):369-375.
Abstract
It is reported that the most abundant polycyclic aromatic hydrocarbons (PAHs) in weathered crude oils are cardiotoxic. However, the action mechanism of PAHs on vertebrate cardiovascular development and disease is unclear. In the present study, the cardiac morphology and functioning of zebrafish embryos exposed to benzo[a]pyrene [B(a)P], as a high-ring PAHs, for 72 h were observed and determined. The results showed that B(a)P exposure resulted in cardiac developmental defects in zebrafish embryos. Significant changes in expression level of multiple genes potentially critical for regulating the B(a)P-induced cardiovascular developmental defects were also found. A gene network regulating cardiac development perturbed by B(a)P exposure was identified and established by computational analysis and employment of some databases. The information from the network could provide a clue for further mechanistic studies explaining molecular events regulating B(a)P-mediated cardiovascular defects and consequences.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping