Abstract

Alcohol is recognized as a classic teratogen capable of inducing a wide range of developmental abnormalities. Alcohol abuse during pregnancy produces permanent brain damage in the fetus and is associated with the development of a life-long behavioral, social, and cognitive disorder now known as fetal alcohol spectrum disorder (FASD). The most clinically recognizable form of FASD is fetal alcohol syndrome (FAS) which is characterized by a set of characteristics including facial dysmorphogenesis, mental dysfunction, growth retardation, and cardiovascular and limb defects. Due to ethical constraints, human studies of FASD are very limited; however, our current understanding of FASD is mainly based on studies on several model vertebrate and invertebrate organisms. The fish embryo, especially zebrafish (Danio rerio) and Japanese medaka (Oryzias latipes), have proven utility for studying ethanol's damaging effects during morphogenesis. These two fish are long-established models for research in developmental biology and have been used to explore ethanol's effect on neurogenesis, cardiogenesis, intracellular signaling, neurobehavioral aspects, and apoptosis. Zebrafish are the center of attraction as a fish model of FASD; however, we have demonstrated that medaka embryos exposed to ethanol during development have several phenotypic features in craniofacial, cardiovascular structures and many biochemical parameters which are comparable to FASD phenotypes observed in human. In this chapter, we reviewed our findings and propose that medaka embryogenesis, like zebrafish, may be a very useful model for investigating the molecular endpoints of FASD.

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