Prenatal ethanol exposure alters adrenocortical development of offspring.
Prenatal ethanol exposure alters adrenocortical development of offspring.
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产前乙醇暴露会改变后代的肾上腺皮质发育。
DOI：
10.1111/j.1530-0277.1989.tb00287.x
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Weinberg,J
中科院分区：
文献类型：
--
作者：
Weinberg,J
产前乙醇和母亲的营养状况对生殖结果和母亲和后代肾上腺皮质活动的相互影响进行了研究。妊娠雌性动物在液态饮食（36%乙醇来源的热量）中给予乙醇，这在妊娠要求方面是边际或最佳的。包括配对喂食和自由喂食对照组。从妊娠第1天至分娩期间摄入乙醇的雌性动物体重增加较少，分娩延迟，并且与配对喂养或对照雌性动物相比，活产幼崽较少且较小，无论其摄入的是边际饲料还是最佳饲料。在妊娠第21天停用乙醇可减轻乙醇对生殖结局的许多不良影响。然而，产前母亲的乙醇摄入量改变肾上腺皮质的活动/反应的母亲，胎儿，和断奶前的后代，无论母亲的营养状况。母体的相对肾上腺重量和基础皮质酮水平在产前和分娩时均增加。在妊娠第21天，乙醇暴露胎仔（A）的相对肾上腺重量增加，但基础皮质酮水平低于配对喂养（PF）和对照（C）胎仔。在出生时，血浆和肾上腺皮质酮水平增加，而绝对肾上腺重量和皮质酮结合球蛋白（CBG）的结合能力在A新生儿下降。在5日龄时，与PF和C幼仔相比，A幼仔在应激后15分钟对乙醚的血浆皮质激素反应降低，在应激后90分钟对新奇物或生理盐水注射的血浆皮质激素反应降低。CBG结合能力也在A幼仔中降低。在10天的年龄，血浆皮质酮水平总体上低于A和PF比在C幼犬暴露于一些不同的急性应激源，而在18天的血浆皮质激素减少，肾上腺皮质酮增加A相比，PF和/或C幼犬。这些数据支持并扩展了以前的研究，表明在子宫内乙醇暴露改变出生后肾上腺皮质发育。这种效应是乙醇特有的，不受母体营养状况的影响。
Interactive effects of prenatal ethanol and maternal nutritional status on reproductive outcome and maternal and offspring adrenocortical activity were examined. Ethanol was administered to pregnant females in liquid diets (36% ethanol‐derived calories) which were marginal or optimal in terms of requirements for pregnancy. Both pair‐fed and ad libitum fed control groups were included. Females consuming ethanol from gestation Day 1 through parturition gained less weight, were delayed in parturition, and had fewer and smaller live born young than pair‐fed or control females, regardless of whether they consumed marginal or optimal diets. Withdrawing ethanol on Day 21 of gestation attenuated many of ethanol's adverse effects on reproductive outcome. However, prenatal maternal ethanol intake altered adrenocortical activity/responsiveness of the mother, the fetus, and the preweaning offspring, regardless of maternal nutritional status. Relative adrenal weights and basal corticos‐terone levels were increased in the dam both prenatally and at parturition. Ethanol‐exposed fetuses (A) had increased relative adrenal weights but lower basal corticosterone levels than pair‐fed (PF) and control (C) fetuses on gestation Day 21. At birth, plasma and adrenal corticosterone levels were increased, while absolute adrenal weights and corticosterone binding globulin (CBG) binding capacity were decreased in A neonates. At 5 days of age, A pups showed reduced plasma corticoid responses to ether at 15 min poststress and to novelty or saline injection at 90‐min post stress compared to PF and C pups. CBG binding capacity was also reduced in A pups. At 10 days of age, plasma corticosterone levels were lower overall in A and PF than in C pups following exposure to a number of different acute stressors while at 18 days plasma corticoids were decreased and adrenal corticosterone was increased in A compared to PF and/or C pups. These data support and extend previous studies indicating that in utero ethanol exposure alters postnatal adrenocortical development. This effect is specific to ethanol and unaltered by maternal nutritional status.