Acrylamide (AA), an environmental pollution and food processing induced chemical contaminant, has been linked to neurotoxicity, genotoxicity and carcinogenicity. However, whether AA exposure may result in developmental disorders in cardiogenesis and related mode of mechanism remain unclear. Here we used zebrafish model to innovatively link AA to cardiac disease etiology about the congenital heart defects. The results showed that treatment of embryonic zebrafish with AA immediately after fertilization specifically resulted in decreasing expressions of nkx2.5, myl7 and vmhc in the anterior lateral plate mesoderm, and then led to abnormal expressions of cardiac myocardium genes by 24 hpf. Furthermore, the cardiac morphogenesis has undergone abnormal process of looping and ballooning by 48 hpf. Although cell apoptosis was not affected, the capacity of cardiomyocyte proliferation was significantly reduced by AA exposure after fertilization. In addition, the differentiation of atrioventricular (AV) canal was dramatically impeded by the over expression of AV boundary markers bmp4, tbx2b and notch1b, which was further confirmed by the ectopic expression of AV valve precursor markers has2, klf2a and nfatc1 at 52 hpf. The study demonstrated that AA-induced cardiotoxicity was related to decreased cardiac progenitor genes expression, reduced myocardium growth, abnormal cardiac chambers morphogenesis and disordered AV canal differentiation. Exposure to AA should be minimized during pregnancy and embryonic development because the cardiogenic period may be vulnerable to AA exposure.

Characterization of acrylamide-induced cardiotoxicity during cardiac progenitor commitment and atrioventricular canal differentiation in zebrafish

254th National Meeting (2017)

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