Prolonged exposure to carbon nanoparticles induced methylome remodeling and gene expression in zebrafish heart.
Animals
Apoptosis
/ drug effects
Cytokines
/ metabolism
DNA Methylation
/ drug effects
Epigenome
/ drug effects
Female
Gene Expression
/ drug effects
Heart
/ drug effects
In Situ Nick-End Labeling
Male
Myocardium
/ immunology
Nanoparticles
/ metabolism
Particle Size
Soot
/ metabolism
Tissue Distribution
Zebrafish
carbon nanoparticles (CNPs)
cardiotoxicity
inflammation
methylome remodeling
zebrafish
Journal
Journal of applied toxicology : JAT
ISSN: 1099-1263
Titre abrégé: J Appl Toxicol
Pays: England
ID NLM: 8109495
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
06
06
2018
revised:
06
08
2018
accepted:
06
08
2018
pubmed:
6
10
2018
medline:
9
6
2020
entrez:
6
10
2018
Statut:
ppublish
Résumé
Growing black carbon (BC) emission has become one of the major urgent environmental issues facing human beings. Usually, BC or BC-containing carbon nanoparticles (CNPs) were recognized as non-directly toxic components of atmospheric particulate matter. However, epidemiology studies have provided much evidence of the associations of exposure of particulate-containing carbon particles with cardiovascular diseases. There are still no related studies to support the epidemiological conclusions. Hence, in this article we exposed adult zebrafish to CNPs for 60 days, and then explored the heart location and potential adverse effects on cardiac tissues of these nanosized carbon particles. Our results first showed direct visualization of cardiac endothelial uptake and heart deposition of CNPs in zebrafish. In addition, CNPs caused significant ultrastructural alterations in myocardial tissue and induced the expression of inflammatory cytokines in a dose-dependent manner, resulting in sub-endocardial inflammation and cell apoptosis. Moreover, our data demonstrated the perturbations caused by CNPs on DNA methylation, suggesting that DNA methylome remodeling might play a critical role in CNP-induced cardiotoxicity in zebrafish heart. Therefore, this study not only proved a laboratory link between CNP exposure and cardiotoxicity in vivo, but also indicated a possible toxicity mechanism involved.
Substances chimiques
Cytokines
0
Soot
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
322-332Informations de copyright
© 2018 John Wiley & Sons, Ltd.