Abstract
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.
Highlights
Chronic alcohol consumption can cause damage to various organs, resulting in different disturbances [1]
Alcohol treated trophoblast cells showed an important increase in the expression of insulin-like grow factor 2 (IGF2) (Figure 2)
It is likely that higher levels of IGF2 allow catch-up growth in children with Foetal Alcohol Syndrome Disorder (FASD) [18]
Summary
Chronic alcohol consumption can cause damage to various organs, resulting in different disturbances [1]. One of the health consequences of alcohol consumption in pregnant women is Foetal Alcohol Syndrome (FAS), a condition resulting from the exposure of the developing embryo to ethanol [2,3]. The clinical features of FAS can be broadly divided into: morphological malformations, especially craniofacial defects, central nervous system impairment, neuropsychological traits, and growth retardation [4,5]. Offspring of mothers who drink heavily during pregnancy can develop FAS with all the symptoms described above, but some cases show no physical or morphological evidences of prenatal alcohol effects at birth [6]. Current estimates suggest that at least 9.1/1000 of the paediatric population has Foetal Alcohol Syndrome Disorder (FASD). A large majority of this group is characterized by adverse neurobehavioral consequences that may be misdiagnosed for years, diminishing the beneficial prospect of earlier interventional opportunities [7,8]
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