Ethanol Increases the Potential for the Generation of Reactive Oxygen Species and Produces Embryotoxicity by Inhibiting Pathways of Histriotrophic Nutrition
Cho, Katherine H.
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Fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASD) are characterized by mental retardation, abnormality of the central nervous system, and facial deformation, affect millions of individuals, but its exact mechanism is unknown. This study investigates the effect of ethanol on pathways of histiotrophic nutrition and the consequences embryonic malnutrition has on cell proliferation. The embryo is nourished via pinocytosis, and following pinocytic uptake, the exogenous matter undergoes proteolysis, and the resulting amino acids are used in protein synthesis in the embryonic and visceral yolk sac (VYS) cells. Malnutrition leads to fewer available amino acids, and less cysteine and its successor, glutathione are produced, leading to free radical formation and a more oxidizing environment, which encourages the initiation of cell death pathways. Whole embryo culture in media containing FITC-Ab and ethanol will allow for visual morphology assessment, and histiotrophic nutrition will be quantified via fluorescent spectroscopy. Free radical generation will be determined through the evaluation of GSH/GSSG levels and measured by HPLC. Decreases in embryonic growth and development as well as the interference of histiotrophic nutrition were observed. Also observed was the dose-dependent increase in the half-cell redox potential, indicating an increasingly oxidizing environment. It is therefore concluded that ethanol increases the potential for generation of reactive oxygen species (ROS) and produces embryotoxicity by inhibiting pathways of histiotrophic nutrition.