Loading…
Benzo[a]pyrene exposure influences the cardiac development and the expression of cardiovascular relative genes in zebrafish (Daniorerio) embryos
► We observed B(a)P exposure resulted in cardiac developmental defects in zebrafish embryos. ► Genes potentially critical for regulating B(a)P-induced cardiovascular developmental defects were identified. ► B(a)P-modulated cardiac development regulating network was predicted. ► These data provided n...
Saved in:
Published in: | Chemosphere (Oxford) 2012-04, Vol.87 (4), p.369-375 |
---|---|
Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | ► We observed B(a)P exposure resulted in cardiac developmental defects in zebrafish embryos. ► Genes potentially critical for regulating B(a)P-induced cardiovascular developmental defects were identified. ► B(a)P-modulated cardiac development regulating network was predicted. ► These data provided novel insight into the molecular actions of B(a)P on the cardiac system.
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 72h 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. |
---|---|
ISSN: | 0045-6535 1879-1298 |
DOI: | 10.1016/j.chemosphere.2011.12.026 |