Effects of acute prenatal ethanol administration in a reciprocal cross of C57BL/6J and short-sleep mice: maternal effects and nonmaternal factors.

Effects of acute prenatal ethanol administration in a reciprocal cross of C57BL/6J and short-sleep mice: maternal effects and nonmaternal factors.
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急性产前乙醇给药对 C57BL/6J 和短睡眠小鼠交互杂交的影响:母体效应和非母体因素。

DOI:
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发表时间:
1997
期刊:
Alcoholism: Clinical and Experimental Research
影响因子:
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通讯作者:
Dawn R. Tweden
Dawn R. Tweden
中科院分区:
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文献类型:
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作者:
David M. Gilliam;Margaret A. Mantle;Deborah A. Barkhausen;Dawn R. Tweden

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一个动物模型被用来观察母体遗传因素是否会导致酒精引起的胎儿畸形。用易感C57BL/6J(B6)和抗短睡眠(SS)小鼠进行正反交设计。本设计产生了四种胎儿基因型:纯种B6B6和SSSS窝产仔以及B6SS和SSB6杂交窝产仔。在怀孕第9天,用5.8克/公斤的乙醇或等卡路里的麦芽糖-糊精插管。在怀孕第18天取出胎儿,并评估软组织和大体畸形。结果显示,不同的胎儿基因型对畸形的产前治疗效果不同。酒精处理组总畸形率分别为61%(B6B6)、28%(B6SS)、3%(SSB6)和16%(SSSS)。暴露在麦芽糖-糊精环境中的小鼠,无论是哪种胎儿,畸形率都很低(或=4%)。遗传相同的杂交后代(B6SS和SSB6)在致畸反应上的差异表明母体遗传对易感性有贡献。在两种主要类型的畸形中,前肢畸形而不是肾脏畸形表现出一种具有母体遗传效应特征的模式。结论:乙醇致畸的母体遗传效应和胎儿遗传效应是可以区分的。母亲对酒精的遗传生理反应可能会给孩子带来不同程度的产前酒精影响风险。
An animal model was used to see if maternal genetic factors contribute to ethanol-induced fetal malformations. Susceptible C57BL/6J (B6) and resistant Short-Sleep (SS) mice were used in a reciprocal cross-breeding design. This design produced four fetal genotypes: true-bred B6B6 and SSSS liters and hybrid B6SS and SSB6 litters. Dams were intubated with either 5.8 g/kg of ethanol or an isocaloric amount of maltose-dextrin on day 9 of pregnancy. Fetuses were removed on day 18 of pregnancy and assessed for soft tissue and gross malformations. Results show different prenatal treatment effects on malformations depending on the fetal genotype. Mean percentage of total malformations in ethanol-treated groups were 61% (B6B6), 28% (B6SS), 3% (SSB6), and 16% (SSSS), respectively. Litters exposed to maltose-dextrin showed low (< or = 4%) malformation rates regardless of fetal genotype. The difference in teratogenic response between genetically identical hybrid litters (B6SS and SSB6) suggests a maternal genetic contribution to susceptibility. Of the two major types of malformations, forelimb but not kidney malformations showed a pattern characteristic of a maternal genetic effect. It was concluded that maternal genetic effects can be distinguished from fetal genetic effects responsible for ethanol teratogenesis. Genetically based physiological responses to alcohol in the mother may confer varying degrees of risk for prenatal alcohol effects in the child.
前列腺素合成抑制剂可阻止酒精引起的胎儿发育不全。
DOI: 10.1111/j.1530-0277.1985.tb05578.x
发表时间: 1985
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