26- Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis. Modulation by nitric oxide.

CEBRAL, E. FALETTI, AB., JAWERBAUM, A., PAZ, D

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS

ELSEVIER

Lugar: Escocia; Año: 2006 vol. 76 p. 141 - 151

0952-3278

The mechanisms of the teratogenic effects of maternal alcohol consumption remain unclear. The aim of the present work was to study the organogenic PGE2 levels and the modulation of PGE2 levels by NO after periconceptional alcohol ingestion. Female mice were intoxicated with a 10% ethanol in drinking water before pregnancy and up to day 10 of gestation. The PGE2 released from organogenic embryos was measured by radio immunoassay following incubation with or without the addition of either a NO donor or a NO synthase (NOS) inhibitor. In the ethanol-treated females, we found increased percentages of retarded embryos, associated with a significantly elevated resorption rate (p<0.05), very high quantities of morphologically abnormal E.10 embryos (p<0.001) and significantly increased PGE2 release, as compared to the embryo parameters of control females. While in the control-derived E.10 embryos the NO donor produced significantly increased PGE2 release, in the ethanol-derived embryos decreased quantities of PGE2 were observed.  L-NMMA inhibited PGE2 release in both control and ethanol-derived embryos at different concentrations, whereas it decreased PGE2 content in controls but not in ethanol-derived embryos. The periconceptional alcohol ingestion produced excessive PGE2 release, decreased PGE2 content and disruption of the regulatory NO-PGE2 pathways. These PGs alterations may be related to delayed organogenesis and abnormal neural tube development after chronic periconceptional consumption of alcohol.