Trichloroethylene Exposure during Cardiac Valvuloseptal Morphogenesis Alters Cushion Formation and Cardiac Hemodynamics in the Avian Embryo
| العنوان: | Trichloroethylene Exposure during Cardiac Valvuloseptal Morphogenesis Alters Cushion Formation and Cardiac Hemodynamics in the Avian Embryo |
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| المؤلفون: | Norman Hu, Stacy Koprowski, John Lough, Susan M. Smith, Victoria J. Drake |
| المصدر: | Environmental Health Perspectives |
| بيانات النشر: | National Institute of Environmental Health Sciences, 2006. |
| سنة النشر: | 2006 |
| مصطلحات موضوعية: | Cardiac function curve, Cardiac output, medicine.medical_specialty, cardiac cushions, trichloroethylene, Health, Toxicology and Mutagenesis, proliferation, Hemodynamics, Apoptosis, Chick Embryo, 010501 environmental sciences, Biology, 01 natural sciences, Doppler ultrasound, 03 medical and health sciences, Internal medicine, medicine, Heart Septum, Morphogenesis, Animals, Incubation, 030304 developmental biology, 0105 earth and related environmental sciences, 0303 health sciences, Heart development, Research, Public Health, Environmental and Occupational Health, Embryo, heart development, Heart septum, Teratology, 3. Good health, Endocrinology, 13. Climate action, embryonic structures |
| الوصف: | It is controversial whether trichloroethylene (TCE) is a cardiac teratogen. We exposed chick embryos to 0, 0.4, 8, or 400 ppb TCE/egg during the period of cardiac valvuloseptal morphogenesis (2-3.3 days' incubation) . Embryo survival, valvuloseptal cellularity, and cardiac hemodynamics were evaluated at times thereafter. TCE at 8 and 400 ppb/egg reduced embryo survival to day 6.25 incubation by 40-50%. At day 4.25, increased proliferation and hypercellularity were observed within the atrioventricular and outflow tract primordia after 8 and 400 ppb TCE. Doppler ultrasound revealed that the dorsal aortic and atrioventricular blood flows were reduced by 23% and 30%, respectively, after exposure to 8 ppb TCE. Equimolar trichloroacetic acid (TCA) was more potent than TCE with respect to increasing mortality and causing valvuloseptal hypercellularity. These results independently confirm that TCE disrupts cardiac development of the chick embryo and identifies valvuloseptal development as a period of sensitivity. The hypercellular valvuloseptal profile is consistent with valvuloseptal heart defects associated with TCE exposure. This is the first report that TCA is a cardioteratogen for the chick and the first report that TCE exposure depresses cardiac function. Valvuloseptal hypercellularity may narrow the cardiac orifices, which reduces blood flow through the heart, thereby compromising cardiac output and contributing to increased mortality. The altered valvuloseptal formation and reduced hemodynamics seen here are consistent with such an outcome. Notably, these effects were observed at a TCE exposure (8 ppb) that is only slightly higher than the U.S. Environmental Protection Agency maximum containment level for drinking water (5 ppb) . |
| اللغة: | English |
| تدمد: | 1552-9924 0091-6765 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::434264d98de3cf1f535baa3ed28df86c http://europepmc.org/articles/PMC1480523 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....434264d98de3cf1f535baa3ed28df86c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15529924 00916765 |
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