| Dietary zinc supplementation throughout pregnancy protects against fetal dysmorphology and improves postnatal survival after prenatal ethanol exposure in mice. | |
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MedLine Citation:
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PMID: 19183140 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: We have previously demonstrated that ethanol teratogenicity is associated with metallothionein-induced fetal zinc (Zn) deficiency, and that maternal subcutaneous Zn treatment given with ethanol in early pregnancy prevents fetal abnormalities and spatial memory impairments in mice. Here we investigated whether dietary Zn supplementation throughout pregnancy can also prevent ethanol-related dysmorphology. METHODS: Pregnant mice were injected with saline or 25% ethanol (0.015 ml/g intraperitoneally at 0 and 4 hours) on gestational day (GD) 8 and fed either a control (35 mg Zn/kg) or a Zn-supplemented diet (200 mg Zn/kg) from GD 0 to 18. Fetuses from the saline, saline + Zn, ethanol and ethanol + Zn groups were assessed for external birth abnormalities on GD 18. In a separate cohort of mice, postnatal growth and survival of offspring from these treatment groups were examined from birth until postnatal day 60. RESULTS: Fetuses from dams treated with ethanol alone in early pregnancy had a significantly greater incidence of physical abnormalities (26%) compared to those from the saline (10%), saline + Zn (9%), or ethanol + Zn (12%) groups. The incidence of abnormalities in ethanol + Zn-supplemented fetuses was not different from saline-treated fetuses. While ethanol exposure did not affect the number of fetal resorptions or pre- or postnatal weight, there were more stillbirths with ethanol alone, and cumulative postnatal mortality was significantly higher in offspring exposed to ethanol alone (35% deaths) compared to all other treatment groups (13.5 to 20.5% deaths). Mice supplemented with Zn throughout pregnancy had higher plasma Zn concentrations than those in un-supplemented groups. CONCLUSIONS: These findings demonstrate that dietary Zn supplementation throughout pregnancy ameliorates dysmorphology and postnatal mortality caused by ethanol exposure in early pregnancy. |
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Authors:
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Brooke L Summers; Allan M Rofe; Peter Coyle |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-01-12 |
Journal Detail:
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Title: Alcoholism, clinical and experimental research Volume: 33 ISSN: 1530-0277 ISO Abbreviation: Alcohol. Clin. Exp. Res. Publication Date: 2009 Apr |
Date Detail:
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Created Date: 2009-04-01 Completed Date: 2009-07-07 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7707242 Medline TA: Alcohol Clin Exp Res Country: England |
Other Details:
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Languages: eng Pagination: 591-600 Citation Subset: IM |
Affiliation:
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Hanson Institute/Institute of Medical and Veterinary Science, Adelaide, SA, Australia. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Abnormalities, Drug-Induced
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prevention & control* Alcoholism / complications Animals Central Nervous System Depressants / adverse effects*, pharmacology Dietary Supplements Disease Models, Animal Embryonic Development / drug effects* Ethanol / adverse effects*, pharmacology Female Liver / metabolism Male Metallothionein / metabolism Mice Mice, Inbred C57BL Pregnancy Pregnancy Outcome Pregnancy, Animal / drug effects* Prenatal Exposure Delayed Effects / chemically induced, prevention & control* Sodium Chloride / pharmacology Zinc / administration & dosage, metabolism, pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Central Nervous System Depressants; 64-17-5/Ethanol; 7440-66-6/Zinc; 7647-14-5/Sodium Chloride; 9038-94-2/Metallothionein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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