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

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...

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Publicado: 2007
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Mus
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09523278_v76_n3_p141_Cebral
http://hdl.handle.net/20.500.12110/paper_09523278_v76_n3_p141_Cebral
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spelling paper:paper_09523278_v76_n3_p141_Cebral2023-06-08T15:55:02Z Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide alcohol drinking water n(g) methylarginine nitric oxide nitric oxide donor nitric oxide synthase inhibitor prostaglandin E alcohol consumption alcohol intoxication animal experiment animal tissue article controlled study embryo embryo development embryo resorption embryopathy female gestation period mouse neural tube neural tube defect nonhuman organogenesis pregnancy priority journal prostaglandin release radioimmunoassay Alcohol Drinking Animals Body Weight Central Nervous System Depressants Embryo Embryo Implantation Embryonic Development Enzyme Inhibitors Ethanol Female Mice Nitric Oxide Donors Nitric Oxide Synthase omega-N-Methylarginine Organogenesis Pregnancy Prostaglandins E Radioimmunoassay Mus 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. © 2007. 2007 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09523278_v76_n3_p141_Cebral http://hdl.handle.net/20.500.12110/paper_09523278_v76_n3_p141_Cebral
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic alcohol
drinking water
n(g) methylarginine
nitric oxide
nitric oxide donor
nitric oxide synthase inhibitor
prostaglandin E
alcohol consumption
alcohol intoxication
animal experiment
animal tissue
article
controlled study
embryo
embryo development
embryo resorption
embryopathy
female
gestation period
mouse
neural tube
neural tube defect
nonhuman
organogenesis
pregnancy
priority journal
prostaglandin release
radioimmunoassay
Alcohol Drinking
Animals
Body Weight
Central Nervous System Depressants
Embryo
Embryo Implantation
Embryonic Development
Enzyme Inhibitors
Ethanol
Female
Mice
Nitric Oxide Donors
Nitric Oxide Synthase
omega-N-Methylarginine
Organogenesis
Pregnancy
Prostaglandins E
Radioimmunoassay
Mus
spellingShingle alcohol
drinking water
n(g) methylarginine
nitric oxide
nitric oxide donor
nitric oxide synthase inhibitor
prostaglandin E
alcohol consumption
alcohol intoxication
animal experiment
animal tissue
article
controlled study
embryo
embryo development
embryo resorption
embryopathy
female
gestation period
mouse
neural tube
neural tube defect
nonhuman
organogenesis
pregnancy
priority journal
prostaglandin release
radioimmunoassay
Alcohol Drinking
Animals
Body Weight
Central Nervous System Depressants
Embryo
Embryo Implantation
Embryonic Development
Enzyme Inhibitors
Ethanol
Female
Mice
Nitric Oxide Donors
Nitric Oxide Synthase
omega-N-Methylarginine
Organogenesis
Pregnancy
Prostaglandins E
Radioimmunoassay
Mus
Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide
topic_facet alcohol
drinking water
n(g) methylarginine
nitric oxide
nitric oxide donor
nitric oxide synthase inhibitor
prostaglandin E
alcohol consumption
alcohol intoxication
animal experiment
animal tissue
article
controlled study
embryo
embryo development
embryo resorption
embryopathy
female
gestation period
mouse
neural tube
neural tube defect
nonhuman
organogenesis
pregnancy
priority journal
prostaglandin release
radioimmunoassay
Alcohol Drinking
Animals
Body Weight
Central Nervous System Depressants
Embryo
Embryo Implantation
Embryonic Development
Enzyme Inhibitors
Ethanol
Female
Mice
Nitric Oxide Donors
Nitric Oxide Synthase
omega-N-Methylarginine
Organogenesis
Pregnancy
Prostaglandins E
Radioimmunoassay
Mus
description 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. © 2007.
title Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide
title_short Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide
title_full Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide
title_fullStr Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide
title_full_unstemmed Periconceptional alcohol consumption-induced changes in embryonic prostaglandin E levels in mouse organogenesis: Modulation by nitric oxide
title_sort periconceptional alcohol consumption-induced changes in embryonic prostaglandin e levels in mouse organogenesis: modulation by nitric oxide
publishDate 2007
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09523278_v76_n3_p141_Cebral
http://hdl.handle.net/20.500.12110/paper_09523278_v76_n3_p141_Cebral
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