Miller M W, Roskams A J, Connor J R
Research Service, Veterans Affairs Medical Center, Iowa City, IA 52242-1057, USA.
J Neurochem. 1995 Jul;65(1):373-80. doi: 10.1046/j.1471-4159.1995.65010373.x.
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 brainstem). 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.
胎儿酒精综合征所产生的缺陷与早期缺铁相关的异常情况相似。因此，我们研究了产前接触乙醇对铁、转铁蛋白和铁蛋白浓度的影响。实验对象是怀孕大鼠的后代，这些大鼠分别被喂食含乙醇的饮食（Et组）、热量相同的对照饮食（Ct组），或普通食物和水。在三个中枢神经系统区域（大脑皮层、皮层下前脑和脑干）评估铁、转铁蛋白和铁蛋白的含量。在对照大鼠的所有三个脑区中，铁、转铁蛋白和铁蛋白水平在出生后的前两周下降，在第3周达到最低水平，然后上升至成年水平。这种模式因乙醇处理而延迟，例如，Et组大鼠中铁、转铁蛋白和铁蛋白的最低浓度比Ct组大鼠出现得更晚（分别晚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，转铁蛋白浓度未受影响，铁蛋白浓度升高。最终结果是，乙醇暴露损害了铁的及时输送和生物利用度。铁调节缺陷是永久性的，可能是乙醇诱导的依赖铁的生长过程（如髓鞘形成）异常的基础。
