Clave S, Joya X, Salat-Batlle J, Martinez SE, Garcia-Algar O and Vall O
Foetal Alcohol Syndrome Disorder (FASD) is a complex condition resulting from the consumption of alcohol during pregnancy. Diagnosis of prenatal exposure to alcohol depends on questionnaire about consumption, biomarkers in neonatal alternative matrices as maternal hair and neonatal meconium, and postnatal clinical data as facial features. However, biomarkers of cellular damage due to exposure to alcohol during pregnancy are lacking. Prenatal alcohol exposure can lead to altered placental cellular function, resulting in changes in hormone production. Herein, the alteration in the synthesis of this hormonal output was studied using a cultured human trophoblast cell line (JEG3). The production of insulin-like grow factor 2 (IGF2), human chorionic gonadotrophin (hCG), human placental lactogen (hPL)
and pregnancy specific glycoprotein 1 (PSG1) was analyzed. Sustained ethanol exposure significantly increased the cellular production and release of IGF2 and hCG in a dose-dependent manner related to the ethanol input. Moreover, ethanol exposure also caused a loss in cell viability and a significant decrease in total protein production. This hormonal alteration may be used in future studies as preliminary candidate to validate surrogate biomarkers of damage.
