IRON REGULATION IN THE DEVELOPING RAT-BRAIN - EFFECT OF IN-UTERO ETHANOL EXPOSURE

Fetal alcohol syndrome produces defects that parallel abnormalities as sociated with early iron deficiency. Hence, we examined the effects of prenatal exposure to ethanol on iron, transferrin, and ferritin conce ntrations. The subjects were the offspring of pregnant rats fed an eth anol-containing diet (Et), pair-fed an isocaloric control diet (Ct), o r fed chow and water. The amounts of iron, transferrin, and ferritin w ere assessed in three CNS regions (cerebral cortex, subcortical forebr ain, and brainstem). in all three segments of the control rats, iron, transferrin, and ferritin levels decreased during the first 2 postnata l weeks, reached a minimum during week 3, and then rose to adult level s. This pattern was delayed by ethanol treatment, e.g., the minimal co ncentrations 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 w as increased. The net result was that the timely delivery and bioavail ability of iron were compromised by ethanol exposure. The defects in i ron regulation are permanent and may underlie ethanol-induced abnormal ities in iron-dependent growth processes such as myelination.