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Characterization of acrylamide-induced oxidative stress and cardiovascular toxicity in zebrafish embryos
[Display omitted] •Acrylamide induced oxidative stress and disordered lipid metabolism.•Acrylamide induced cardiovascular toxicity with deficient heart morphology and function.•Acrylamide reduced cardiomyocyte proliferation but not apoptosis.•Acrylamide disordered atrioventricular canal differentiat...
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Published in: | Journal of hazardous materials 2018-04, Vol.347, p.451-460 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | [Display omitted]
•Acrylamide induced oxidative stress and disordered lipid metabolism.•Acrylamide induced cardiovascular toxicity with deficient heart morphology and function.•Acrylamide reduced cardiomyocyte proliferation but not apoptosis.•Acrylamide disordered atrioventricular canal differentiation and valve development.
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. |
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ISSN: | 0304-3894 1873-3336 |
DOI: | 10.1016/j.jhazmat.2018.01.016 |