Preterm fetal restriction and malformations induced by periconceptional alcohol ingestion during the first half of pregnancy in CD-1 mouse

PEREZ TITO L; FIGUEIRA MENDES C; MORAES S; CEBRAL E; BEVILACQUA E

Congreso; XV Congresso da Sociedade Brasileira de Biologia Celular (SBBC),; 2010

Sociedade Brasileira de Biologia Celular

Gestational ethanol consumption disrupts fetal development increasing the teratogenic outcomes. The objective was to study the potencial deleterious actions of perigestational alcohol ingestion up to first half of pregnancy on fetal growth and external malformations. Adult CD-1 females were exposed to 10% ethanol for 15 days previous to and during 4 (TF-D4), 8 (TF-D8) or 10 (TF-D10) days of gestation, following replacement ethanol by water up to day 18 of pregnancy. Control group (CF) was performed with water. Fetus and placentae were weighted, measured and fixed for external malformations and skeletal alizarin red evaluation. Mean fetal weight was reduced in TF-D10 vs CF-D10 (p<0,05). The % of malformed fetus was increased in all treated groups (TF-D4 and TF-D10: p<0,001; TF-D8: p=0,001, vs CF), where TF-D4 had the highest % values (92% vs 12.5%). The main malformations were: TF-D4: facial anomalies, TF-D8: facial and member anomalies, TF-D10: craniofacial, members, lower abdominal wall, while CF had minor facial anomalies (ear implantation defect). Cranial skeletal defects (exencephaly) was confirmed by Alizarin analysis. The placental weights decreased in TF-D4 and TF-D10 vs CF (p<0.05). In conclusion, perigestational ingestion of moderate ethanol concentrations up to 4, 8 or 10 day of pregnancy induce at day 18 of gestation, fetal growth restriction and important external craniofacial malformations. Although the period of alcohol exposure more susceptible for fetal growth retardation and dysmorphology was at organogenesis, alcohol ingestion at preimplantation induced facial defects suggesting sensibility of this early gestational phase in the present mouse model.