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Fetal alcohol spectrum disorders (FASD) describe many of the well-known neurodevelopmental deficits afflicting children exposed to alcohol in utero. The effects of alcohol on the maternal-fetal interface, especially the placenta, have been less explored. We herein hypothesized that chronic binge alcohol exposure during pregnancy significantly alters the placental protein profile in a rat FASD model
Pregnant rats were orogastrically treated daily with alcohol (4.5 g/kg, gestational day (GD) 5-10; 6.0 g/kg, GD 11-19) or 50% maltose dextrin (isocalorically matched pair-fed controls). On GD 20, placentae were collected, flash frozen, and stored until tissues were homogenized. Protein lysates were denatured, reduced, captured on a 10 kDa spin filter and digested. Peptides were eluted, reconstituted, and analyzed by a Q Exactive(™) Hybrid Quadrupole-Orbitrap(™) mass spectrometer
Mass spectrometry analysis identified 2,285 placental proteins based on normalized spectral counts and 2000 proteins by intensity based absolute quantification. 45 placental proteins were significantly (P<0.05) altered by gestational alcohol exposure by both quantification approaches. These included proteins directly related to alcohol metabolism; specific isoforms of alcohol dehydrogenase and aldehyde dehydrogenase were upregulated in the alcohol group. Ingenuity analysis identified ethanol degradation as the most significantly altered canonical pathway in placenta, and fetal/organ development as most altered function, with increased risk for metabolic, neurological, and cardiovascular diseases. Physiologic roles of the significantly altered proteins were related to early pregnancy adaptations, implantation, gestational diseases, fetal organ development, neurodevelopment, and immune functions
We conclude that the placenta is a valuable organ not only to understand FASD etiology but it may also serve as a diagnostic tool to identify novel biomarkers for detecting the outcome of fetal alcohol exposure. Placental mass spectrometry analysis can offer sophisticated insights into identifying alcohol metabolism-related enzymes and regulators of fetal development. This article is protected by copyright. All rights reserved.
This article was published in the following journal.
Name: Alcoholism, clinical and experimental research
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An umbrella term used to describe a pattern of disabilities and abnormalities that result from fetal exposure to ETHANOL during pregnancy. It encompasses a phenotypic range that can vary greatly between individuals, but reliably includes one or more of the following: characteristic facial dysmorphism, FETAL GROWTH RETARDATION, central nervous system abnormalities, cognitive and/or behavioral dysfunction, BIRTH DEFECTS. The level of maternal alcohol consumption does not necessarily correlate directly with disease severity.
Exchange of substances between the maternal blood and the fetal blood at the PLACENTA via PLACENTAL CIRCULATION. The placental barrier excludes microbial or viral transmission.
A condition occurring in FETUS or NEWBORN due to in utero ETHANOL exposure when mother consumed alcohol during PREGNANCY. It is characterized by a cluster of irreversible BIRTH DEFECTS including abnormalities in physical, mental, and behavior development (such as FETAL GROWTH RETARDATION; MENTAL RETARDATION; ATTENTION DEFICIT AND DISRUPTIVE BEHAVIOR DISORDERS) with varied degree of severity in an individual.
A highly vascularized mammalian fetal-maternal organ and major site of transport of oxygen, nutrients, and fetal waste products. It includes a fetal portion (CHORIONIC VILLI) derived from TROPHOBLASTS and a maternal portion (DECIDUA) derived from the uterine ENDOMETRIUM. The placenta produces an array of steroid, protein and peptide hormones (PLACENTAL HORMONES).
A malignant metastatic form of trophoblastic tumors. Unlike the HYDATIDIFORM MOLE, choriocarcinoma contains no CHORIONIC VILLI but rather sheets of undifferentiated cytotrophoblasts and syncytiotrophoblasts (TROPHOBLASTS). It is characterized by the large amounts of CHORIONIC GONADOTROPIN produced. Tissue origins can be determined by DNA analyses: placental (fetal) origin or non-placental origin (CHORIOCARCINOMA, NON-GESTATIONAL).
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