IFIBYNE   05513
INSTITUTO DE FISIOLOGIA, BIOLOGIA MOLECULAR Y NEUROCIENCIAS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Nitric oxide and its relation with prostaglandin E in murine early embryo organogenesis after perigestational alcohol consumption
Autor/es:
COLL, TA., SOBARZO, C., PAZ, D., CEBRAL, E.
Lugar:
Buenos Aires, Argentina
Reunión:
Jornada; VIII Jornadas Multidisciplinarias de la Sociedad Argentina de Biología; 2006
Institución organizadora:
Sociedad Argentina de Biología
Resumen:
Maternal alcohol consumption produces increased early pregnancy loss and teratogenic effects. The prenatal pathogenesis of CNS produced by perigestational alcohol ingestion has not been studied. Nitric oxide (NO) regulates cell survival, apoptosis and differentiation, and interacts with prostaglandin (PG) system, while altered NO levels may contibute to neurodegeneration.The aim was to study the NO in organogenic embryos and the alterations of PGE-NO interrelationship involved in defective neurogenesis after prenatal alcohol ingestion. Female mice were intoxicated with 10 % ethanol in drinking water for 15 days before and during pregnancy up to day 10 (T). Control females received maltose-dextrin in water (C). T had increased abnormal % of E.10 stage embryos (30% vs 10.7%, p<0.001), with defective neural tube (NT) closure (scanning microscopy), altered neuroepithelium, reduced mitotic cell Nr (HyE) and diminished body-cephalic proportion (C:0.5±0.02 vs. T:0.4± 0.01, p<0.05). Endogenous Nitrites (Ni) levels (Griess reaction, kit) were significantly reduced in E.10 embryos from T compared to those of C (p<0.01), which correlated with altered NT neuroepithelial pattern of immunostaining of nNOS. Embryo incubations with NO-donors (Nonoate), NOS inhibitors (L-NMMA) or COX-2 inhibitors (Meloxicam) demonstrated that interrelationship NO-PGE (RIA) and PGE-NO resulted deregulated in T-derived embryos while C-embryos had a positive modulation. In conclusion, deficient NO levels after maternal alcohol ingestion may lead to embryofetal microcephaly due to deregulation of PG-NO pathway that participate in neuronal proliferation and differentiation of early NT development.