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母体摄入乙醇对胎鼠脑维生素A的影响:胎儿酒精综合征的一个模型

Maternal ethanol ingestion effects on fetal rat brain vitamin A as a model for fetal alcohol syndrome.

作者信息

Grummer M A, Langhough R E, Zachman R D

机构信息

Department of Pediatrics, University of Wisconsin-Meriter Perinatal Center, Madison 53715.

出版信息

Alcohol Clin Exp Res. 1993 Jun;17(3):592-7. doi: 10.1111/j.1530-0277.1993.tb00805.x.

DOI:10.1111/j.1530-0277.1993.tb00805.x
PMID:8333589
Abstract

Fetal embryo, head, and brain tissue from different gestational ages were analyzed for retinol content, nuclear retinoic acid receptor and cytosolic retinoic acid binding protein levels after maternal ethanol ingestion and compared with fetal levels in control diet pregnancies. Retinol levels in fetal embryo and brain of ethanol-ingesting pregnancies were 2- to 3-fold higher than fetal embryo and brain retinol of control pregnancies. Nuclear retinoic acid receptor was lower in 10-day embryo of ethanol pregnancies and apparently unaffected in fetal head and brain by maternal ethanol consumption at other days of gestation. In fetal head there was a significant overall ethanol effect on cytosolic retinoic acid binding protein, with increased levels in fetal tissue from ethanol-consuming pregnancies. These observations of altered embryo, fetal head, and fetal brain retinol and receptor protein levels support the hypothesis of a possible role of vitamin A in fetal alcohol syndrome.

摘要

对来自不同孕周的胎儿胚胎、头部和脑组织进行分析,测定母体摄入乙醇后其中视黄醇的含量、细胞核视黄酸受体和胞质视黄酸结合蛋白的水平,并与对照组饮食妊娠的胎儿水平进行比较。摄入乙醇的妊娠中胎儿胚胎和脑内的视黄醇水平比对照组妊娠的胎儿胚胎和脑内视黄醇水平高2至3倍。乙醇妊娠10天胚胎中的细胞核视黄酸受体较低,而在妊娠其他天数,母体摄入乙醇对胎儿头部和脑内该受体显然没有影响。在胎儿头部,乙醇对胞质视黄酸结合蛋白有显著的总体影响,摄入乙醇的妊娠胎儿组织中该蛋白水平升高。这些关于胚胎、胎儿头部和胎儿脑内视黄醇及受体蛋白水平改变的观察结果支持了维生素A在胎儿酒精综合征中可能起作用的假说。

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Maternal ethanol ingestion effects on fetal rat brain vitamin A as a model for fetal alcohol syndrome.母体摄入乙醇对胎鼠脑维生素A的影响:胎儿酒精综合征的一个模型
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Hypothesis: prenatal ethanol-induced birth defects and retinoic acid.假设:产前乙醇诱导的出生缺陷与视黄酸
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Alcohol dehydrogenase as a critical mediator of retinoic acid synthesis from vitamin A in the mouse embryo.酒精脱氢酶作为小鼠胚胎中维生素A合成视黄酸的关键介质。
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Ethanol elevates physiological all-trans-retinoic acid levels in select loci through altering retinoid metabolism in multiple loci: a potential mechanism of ethanol toxicity.乙醇通过改变多个部位的视黄醇代谢,使生理全反式视黄酸水平在特定部位升高:这是乙醇毒性的一个潜在机制。
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Ethanol impairs activation of retinoic acid receptors in cerebellar granule cells in a rodent model of fetal alcohol spectrum disorders.乙醇在胎儿酒精谱系障碍的啮齿动物模型中损害小脑颗粒细胞中维甲酸受体的激活。
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Ethanol elevates physiological all-trans-retinoic acid levels in select loci through altering retinoid metabolism in multiple loci: a potential mechanism of ethanol toxicity.乙醇通过改变多个部位的视黄醇代谢,使生理全反式视黄酸水平在特定部位升高:这是乙醇毒性的一个潜在机制。
FASEB J. 2010 Mar;24(3):823-32. doi: 10.1096/fj.09-141572. Epub 2009 Nov 4.
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Role of various neurotransmitters in mediating the long-term endocrine consequences of prenatal alcohol exposure.多种神经递质在介导产前酒精暴露的长期内分泌后果中的作用。
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Gestational exposure to ethanol suppresses msx2 expression in developing mouse embryos.孕期接触乙醇会抑制发育中小鼠胚胎中的msx2表达。
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