INVESTIGADORES
CEBRAL Elisa
artículos
Título:
Abnormal growth and morphogenesis of placenta at term is linked to adverse fetal development after perigestational alcohol consumption up to early gestation in mouse
Autor/es:
GUALDONI, GISELA SOLEDAD; PEREZ TITO L; BARRIL C; SOBARZO C; CEBRAL E
Revista:
Birth Defects Research
Editorial:
Wiley
Referencias:
Año: 2022 p. 1 - 20
ISSN:
2472-1727
Resumen:
Background: Gestation alcohol consumption produces fetal growth restrictionand malformations by affecting the embryo–fetal development. Recentlya relationship between abnormal placentation and fetal malformation andintrauterine growth retardation has been suggested. However, the effects ofperigestational alcohol ingestion up to early pregnancy on the placenta atterm and its association with fetal abnormalities are little known.Methods: In female mice, ethanol 10% in water was administered for 15 daysprevious and up to days 4 (D4), 8 (D8), or 10 (D10) of gestation (TF), and gestationcontinues without ethanol exposure. Control females (CF) received ethanol-freewater. At day 18, feto-placental units and implantation sites were studied.Results: TF had increased resorptions and only fetuses from D8-TF andD10-TF had significantly increased weights versus CF. D4 and D10-TFplacentashad significantly reduced weights. All TF had increased junctionalzone (JZ) and reduced labyrinth (Lab) areas (PAS-histology and morphometry)compared with CF. Fetuses with mainly with craniofacial abnormalities andskeletal defects (Alizarin red staining), significantly increase; while the fetalbone density (alizarin color intensity, ImageJ) was reduced in D4, D8 andD10-TF versus CF. Although all TF-placentas were histo-structural affected,TF-abnormal fetuses had the most severe placental anomalies, with junctionalabundant glycogenic cells into the labyrinth, disorganized labyrinthine vascularizationwith signs of leukocyte infiltrates and feto-maternal blood mix.Conclusions: Perigestational alcohol consumption up to early gestationinduces at term fetal growth alterations, dysmorphology and defective skeleton,linked to deficient growth and abnormal morphogenesis of placenta,highlighting insight into the prenatal etiology of FASD.