Iron regulation in the developing rat brain: effect of in utero ethanol exposure.

Iron regulation in the developing rat brain: effect of in utero ethanol exposure.
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发育中的大鼠大脑中的铁调节:子宫内乙醇暴露的影响。

DOI:
10.1046/j.1471-4159.1995.65010373.x
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发表时间:
1995
影响因子:
4.7
通讯作者:
Connor,JR
Connor,JR
中科院分区:
医学2区
文献类型:
--
作者:
Miller,MW;Roskams,AJ;Connor,JR

文献摘要

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胎儿酒精综合征产生的缺陷与早期缺铁相关的异常平行。因此,我们研究了产前暴露于乙醇对铁,转铁蛋白和铁蛋白浓度的影响。受试者是喂食含乙醇饲料(Et)、成对喂食等热量对照饲料(Ct)或喂食饲料和水的妊娠大鼠的后代。在三个CNS区域(大脑皮质、皮质下前脑和脑干)中评估铁、转铁蛋白和铁蛋白的量。在所有三个部分的控制大鼠,铁,转铁蛋白和铁蛋白水平下降,在出生后的前2周,在第3周达到最低值,然后上升到成人水平。这种模式被乙醇处理延迟,例如,Et给药大鼠中铁、转铁蛋白和铁蛋白的最低浓度比Ct给药大鼠晚达到(分别为3天、7天和2周)。乙醇诱导的铁稳态改变持续到成年期;铁浓度降低,转铁蛋白浓度不受影响,铁蛋白浓度增加。最终结果是,铁的及时输送和生物利用度受到乙醇暴露的影响。铁调节的缺陷是永久性的,可能是乙醇诱导的铁依赖性生长过程异常(如髓鞘形成)的基础。
Fetal alcohol syndrome produces defects that parallel abnormalities associated with early iron deficiency. Hence, we examined the effects of prenatal exposure to ethanol on iron, transferrin, and ferritin concentrations. The subjects were the offspring of pregnant rats fed an ethanol‐containing diet (Et), pair‐fed an isocaloric control diet (Ct), or fed chow and water. The amounts of iron, transferrin, and ferritin were assessed in three CNS regions (cerebral cortex, subcortical forebrain, and brain‐stem). In all three segments of the control rats, iron, transferrin, and ferritin levels decreased during the first 2 postnatal weeks, reached a minimum during week 3, and then rose to adult levels. This pattern was delayed by ethanol treatment, e.g., the minimal concentrations in iron, transferrin, and ferritin in the Et‐treated rats were achieved later (3 days, 7 days, and 2 weeks, respectively) than they were in the Ct‐treated rats. Ethanol‐induced alterations in iron homeostasis persisted into adulthood; iron concentration was reduced, transferrin concentration was unaffected, and ferritin concentration was increased. The net result was that the timely delivery and bioavailability of iron were compromised by ethanol exposure. The defects in iron regulation are permanent and may underlie ethanol‐induced abnormalities in iron‐dependent growth processes such as myelination.