Perspectives On Ethanol Toxicity In Medaka Embryogenesis And Possible Protection By Asian Ginseng (Panax Ginseng): Histological And Biochemical Analysis
Alcohol is recognized as a classic teratogen capable of inducing a wide range of developmental abnormalities. Alcohol consumption during pregnancy may produce 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 specific features including facial dysmorphogenesis, mental dysfunction, growth retardation, and cardiovascular and limb defects. Due to ethical constraints, human studies of FASD are very limited. Therefore our current understanding of FASD is mainly based on several animal models (vertebrate and invertebrate). The fish embryo, especially zebrafish (Danio rerio) and Japanese medaka ( Oryzias latipes), are long-established models for research in developmental biology and have been used to explore alcohol's effect on neurogenesis, cardiogenesis, intracellular signaling, neurobehavioral aspects, and apoptosis. These two fish models have proven utility for studying alcohol's damaging effects during morphogenesis. In this study we have demonstrated that exposing Japanese medaka embryos to alcohol during development shophenotypic features and biochemical parameters that are comparable to FASD phenotypes observed in humans. Asian ginseng (PG) root extract has been shown to have anti alcoholic activities in a number of studies. In this study we have used medaka embryos to induce FASD like neurological defects. We have also investigated the ability of Asian ginseng (PG) to function as a preventive agent of these defects. Our findings suggest that medaka embryogenesis, can be a very useful model for investigating the molecular and morphological endpoints of FASD, and that PG root extract has a protective effect against alcohol induced toxicity in medaka embryogenesis.
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