PUBLICATION
Characterization of acrylamide-induced oxidative stress and cardiovascular toxicity in zebrafish embryos
- Authors
- Huang, M., Jiao, J., Wang, J., Xia, Z., Zhang, Y.
- ID
- ZDB-PUB-180122-3
- Date
- 2018
- Source
- Journal of hazardous materials 347: 451-460 (Journal)
- Registered Authors
- Keywords
- Acrylamide, Cardiovascular, Developmental toxicity, Oxidative stress, Zebrafish embryos
- MeSH Terms
-
- Acrylamide/toxicity*
- Animals
- Apoptosis/drug effects
- Cell Differentiation/drug effects
- Cell Proliferation/drug effects
- Embryo, Nonmammalian/abnormalities
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/physiology
- Heart/drug effects*
- Heart/embryology
- Heart/physiology
- Myocardium/metabolism
- Oxidative Stress/drug effects*
- Zebrafish/abnormalities
- Zebrafish/physiology
- Zebrafish Proteins/metabolism
- PubMed
- 29353190 Full text @ J. Hazard. Mater.
Citation
Huang, M., Jiao, J., Wang, J., Xia, Z., Zhang, Y. (2018) Characterization of acrylamide-induced oxidative stress and cardiovascular toxicity in zebrafish embryos. Journal of hazardous materials. 347:451-460.
Abstract
Acrylamide (AA) is a high production volume chemical in industrial applications and widely found in baked or fried carbohydrate-rich foods. In this study, we unravelled that AA induced developmental toxicity associated with oxidative stress status and disordered lipid distribution in heart region of developing zebrafish. Treatment with AA caused a deficient cardiovascular system with significant heart malformation and dysfunction. We also found that AA could reduce the number of cardiomyocytes through the reduced capacity of cardiomyocyte proliferation rather than cell apoptosis. The cardiac looping and ballooning appeared abnormal though cardiac chamber-specific identity in the differentiated myocardium was maintained well after AA treatment through MF20/S46 immunofluorescence assay. Furthermore, treatment with AA disturbed the differentiation of atrioventricular canal, which was demonstrated by the disordered expressions of the atrioventricular boundary markers bmp4, tbx2b and notch1b and further confirmed by the ectopic expressions of the cardiac valve precursor markers has2, klf2a and nfatc1 through whole-mount in situ hybridization. Thus, our studies provide the evidence of cardiac developmental toxicity of AA in the cardiovascular system, and also raised health concern about the harm of trans-placental exposure to high level of AA for foetuses and the risk of high exposure to AA for the pregnant women.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping