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

Michael W. Miller, A. Jane I. Roskams, James R. Connor

Research output: Contribution to journalArticlepeer-review

46 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)373-380
Number of pages8
JournalJournal of neurochemistry
Issue number1
StatePublished - Jul 1995

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience


Dive into the research topics of 'Iron regulation in the developing rat brain: Effect of in utero ethanol exposure'. Together they form a unique fingerprint.

Cite this