Abstract
Experiments performed with Holtzman rats demonstrated that brain iron (Fe) was lower by postnatal day 13 (P13) in pups born and nursed by dams that began copper-deficient (-Cu) treatment at embryonic day 7. Transcardial perfusion of P24-P26 males and females to remove blood Fe contamination revealed that brain Fe was still 20% lower in -Cu than +Cu rats. Estimated blood content of brain for -Cu rats was greater than for +Cu rats; for all groups, values ranged between 0.43 and 1.03%. Using group-specific data and regression analyses, r = 0.99, relating blood Fe to hemoglobin, brain Fe in non-perfused rats in a replicate study was lower by 33% at P13 and 39% at P24 in -Cu rats. Brain extracts from these rats and from P50 rats from a post-weaning model were compared by immunoblotting for transferrin receptor (TfR1). P24 brain -Cu/+Cu TfR1 was 3.08, suggesting that brains of -Cu rats were indeed Fe deficient. This ratio in P13 rats was 1.44, p < 0.05. No change in P50 -Cu rat brain TfR1 or Fe content was detected despite a 50% reduction in plasma Fe. The results suggest that brain Fe accumulation depends on adequate Cu nutriture during perinatal development.