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Updated: May 14, 2026
Using Chicken Embryo as a Powerful Tool in Assessment of Developmental Cardiotoxicities
Published on: March 21, 2021
The effects of an environmentally relevant 58-congener polychlorinated biphenyl (PCB) mixture on cardiac development
Tiffany Carro1, Lisa A Taneyhill, Mary Ann Ottinger
1Department of Animal and Avian Sciences, University of Maryland, College Park, Maryland, USA. tcarro@gmail.com
Insights
Exposure to polychlorinated biphenyls (PCBs) in ovo caused heart defects in chick embryos. PCB exposure reduced cardiomyocyte proliferation, impacting heart development and morphology.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Cardiovascular Research
Background:
- Polychlorinated biphenyls (PCBs) are persistent environmental pollutants known to cause developmental toxicity.
- Embryonic development, particularly heart formation, is sensitive to chemical exposures.
- Understanding PCB effects on avian embryonic development is crucial for ecological risk assessment.
Purpose of the Study:
- To investigate the teratogenic effects of a specific 58-congener PCB mixture on chicken embryonic heart development.
- To determine the impact of PCB exposure on cardiac protein expression and cellular apoptosis.
- To assess the effect of PCB exposure on cardiomyocyte proliferation during critical developmental stages.
Main Methods:
- In ovo injection of chicken embryos with a 58-congener PCB mixture at Hamburger-Hamilton (HH) stages 10, 16, and 20.
- Monitoring embryo mortality and observing gross heart morphology.
- Histological analysis of cardiac proteins (ventricular myosin heavy chain, titin) and assessment of cellular apoptosis.
- Quantification of cardiomyocyte proliferation rates.
Main Results:
- PCB exposure led to increased embryo mortality and a significant incidence of cardiomyopathies.
- Observed heart abnormalities included abnormal heart tube elongation, improper looping, ventricular wall indentations, and irregular heart shape.
- No significant differences were found in spatiotemporal expression of cardiac proteins or cellular apoptosis.
- A dramatic decline in cardiomyocyte proliferation rates was observed with increasing PCB concentrations.
Conclusions:
- In ovo exposure to the studied PCB mixture adversely affects chicken embryonic heart development.
- Reduced cardiomyocyte proliferation is a key mechanism by which PCBs induce cardiac teratogenicity.
- These findings highlight the risks of PCB contamination to developing avian cardiovascular systems.
Abstract:
Chicken (Gallus domesticus) embryonic exposure in ovo to a 58-congener polychlorinated biphenyl (PCB) mixture resulted in teratogenic heart defects in chick embryos at critical heart developmental stages Hamburger-Hamilton (HH) stages 10, 16, and 20. The 58-congener mixture contained relative proportions of primary congeners measured in belted sandpiper (Megaceryle alcyon) and spotted sandpiper (Actitis macularia) eggs collected along the upper Hudson River, New York, USA, and chicken doses were well below observed environmental exposure levels. Embryos were injected with 0.08 µg PCBs/g egg weight and 0.50 µg PCBs/g egg weight (0.01 and 0.064 ng toxic equivalent/g, respectively) at embryonic day 0, prior to incubation. Mortality of exposed embryos was increased at all developmental stages, with a marked rise in cardiomyopathies at HH16 and HH20 (p < 0.05). Heart abnormalities occurred across all treatments, including abnormal elongation and expansion of the heart tube at HH10, improper looping and orientation, indentations in the emerging ventricular wall (HH16 and HH20), and irregularities in overall heart shape (HH10, HH16, and HH20). Histology was conducted on 2 cardiac proteins critical to embryonic heart development, ventricular myosin heavy chain and titin, to investigate potential mechanistic effects of PCBs on heart development, but no difference was observed in spatiotemporal expression. Similarly, cellular apoptosis in the developing heart was not affected by exposure to the PCB mixture. Conversely, cardiomyocyte proliferation rates dramatically declined (p < 0.01) at HH16 and HH20 as PCB exposure concentrations increased. Early embryonic cardiomyocyte proliferation contributes to proper formation of the morphology and overall thickness of the ventricular wall. Therefore, in ovo exposure to this 58-congener PCB mixture at critical stages adversely affects embryonic heart development.
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