Next Article in Journal
Evidence of Biomass Smoke Exposure as a Causative Factor for the Development of COPD
Previous Article in Journal
Using a Particle Counter to Inform the Creation of Similar Exposure Groups and Sampling Protocols in a Structural Steel Fabrication Facility
Previous Article in Special Issue
Occupational Exposure to Bisphenol A (BPA): A Reality That Still Needs to Be Unveiled
Article

Embryonic Ethanol Exposure Affects Early- and Late-Added Cardiac Precursors and Produces Long-Lasting Heart Chamber Defects in Zebrafish

Department of Biology, Indiana University Purdue University Indianapolis, 723 West Michigan, Indianapolis, IN 46202, USA
*
Authors to whom correspondence should be addressed.
Academic Editor: David R. Wallace
Toxics 2017, 5(4), 35; https://doi.org/10.3390/toxics5040035
Received: 27 October 2017 / Revised: 20 November 2017 / Accepted: 22 November 2017 / Published: 1 December 2017
(This article belongs to the Special Issue Reproductive and Developmental Toxicology)
Drinking mothers expose their fetuses to ethanol, which produces birth defects: craniofacial defects, cognitive impairment, sensorimotor disabilities and organ deformities, collectively termed as fetal alcohol spectrum disorder (FASD). Various congenital heart defects (CHDs) are present in FASD patients, but the mechanisms of alcohol-induced cardiogenesis defects are not completely understood. This study utilized zebrafish embryos and older larvae to understand FASD-associated CHDs. Ethanol-induced cardiac chamber defects initiated during embryonic cardiogenesis persisted in later zebrafish life. In addition, myocardial damage was recognizable in the ventricle of the larvae that were exposed to ethanol during embryogenesis. Our studies of the pathogenesis revealed that ethanol exposure delayed differentiation of first and second heart fields and reduced the number of early- and late-added cardiomyocytes in the heart. Ethanol exposure also reduced the number of endocardial cells. Together, this study showed that ethanol-induced heart defects were present in late-stage zebrafish larvae. Reduced numbers of cardiomyocytes partly accounts for the ethanol-induced zebrafish heart defects. View Full-Text
Keywords: fetal alcohol spectrum disorder; congenital heart defects; cardiac defects in zebrafish; ethanol exposure fetal alcohol spectrum disorder; congenital heart defects; cardiac defects in zebrafish; ethanol exposure
Show Figures

Figure 1

MDPI and ACS Style

Sarmah, S.; Marrs, J.A. Embryonic Ethanol Exposure Affects Early- and Late-Added Cardiac Precursors and Produces Long-Lasting Heart Chamber Defects in Zebrafish. Toxics 2017, 5, 35. https://doi.org/10.3390/toxics5040035

AMA Style

Sarmah S, Marrs JA. Embryonic Ethanol Exposure Affects Early- and Late-Added Cardiac Precursors and Produces Long-Lasting Heart Chamber Defects in Zebrafish. Toxics. 2017; 5(4):35. https://doi.org/10.3390/toxics5040035

Chicago/Turabian Style

Sarmah, Swapnalee, and James A. Marrs 2017. "Embryonic Ethanol Exposure Affects Early- and Late-Added Cardiac Precursors and Produces Long-Lasting Heart Chamber Defects in Zebrafish" Toxics 5, no. 4: 35. https://doi.org/10.3390/toxics5040035

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop