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Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
Published on: March 20, 2012
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Angiogenesis is repressed by ethanol exposure during chick embryonic development.
Guang Wang1,2, Shan Zhong1, Shi-yao Zhang1
1Division of Histology and Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, People's Republic of China.
Journal of Applied Toxicology : JAT
|July 17, 2015
Summary
Excess ethanol exposure during pregnancy inhibits embryonic blood vessel formation (angiogenesis) by increasing reactive oxygen species (ROS). This study reveals a direct link between ethanol, ROS, and developmental anti-angiogenesis in chick embryos.
Area of Science:
- Developmental Biology
- Toxicology
- Cardiovascular Research
Background:
- Excess alcohol consumption during pregnancy is linked to Fetal Alcohol Syndrome.
- The direct impact of ethanol on embryonic angiogenesis remains unclear.
Purpose of the Study:
- To investigate the direct effect of ethanol on embryonic angiogenesis.
- To determine the role of reactive oxygen species (ROS) in ethanol-induced anti-angiogenesis.
Main Methods:
- Chick yolk sac membrane (YSM) model used for in ovo studies.
- Ethanol and ROS inducer (2,2'-azobis-amidinopropane dihydrochloride) exposure.
- Measurement of antioxidant enzyme activities and gene expression (VEGF, FGF2, HIF).
Main Results:
- Ethanol significantly inhibited angiogenesis in a dose-dependent manner.
- Ethanol exposure increased ROS production, indicated by altered enzyme activities.
- Gene expression of key angiogenesis factors (VEGF, FGF2, HIF) was repressed.
Conclusions:
- Excess ethanol directly inhibits embryonic angiogenesis.
- Ethanol-induced ROS production is a key mechanism underlying this anti-angiogenic effect.
- Findings highlight potential risks of prenatal alcohol exposure to vascular development.
