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Rat brain iron concentration is lower following perinatal copper deficiency
Author(s) -
Prohaska Joseph R.,
Gybina Anna A.
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03091.x
Subject(s) - weaning , medicine , hemoglobin , transferrin receptor , endocrinology , transferrin , chemistry , copper , organic chemistry
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 immunobloting 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.