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Biochemical, Molecular, and Genetic Mechanisms

Iron Injection Restores Brain Iron and Hemoglobin Deficits in Perinatal Copper-Deficient Rats^1,2

Department of Biochemistry and Molecular Biology, University of Minnesota Medical School, Duluth, MN 55812

^* To whom correspondence should be addressed. E-mail: jprohask{at}d.umn.edu.

Copper (Cu) deficiency during perinatal development in rats is associated with anemia, lower plasma iron (Fe), and brain Fe. Experiments were conducted to inject Fe dextran into Cu-deficient (Cu–) rat pups to attempt to reverse these conditions. Previous work with older Cu– rats did not reverse anemia following Fe injection. Dams began Cu-adequate (Cu+) or Cu– dietary treatments starting at embryonic d 7 and lasting through weaning. In Expt. 1, pups from each dietary treatment were given a single dose of Fe, 20 mg Fe/kg, or saline (S) at postnatal d 11 (P11). Plasma Fe and hemoglobin were higher in the Fe-injected groups at P13. Brain Fe deficit and brain transferrin receptor enhancement were eliminated in the Cu– group injected with Fe compared with Cu–S pups, supporting an association between low plasma Fe and low brain Fe. In Expt. 2, Fe treatment was increased to 45 mg Fe/kg. Four injections were given between P5 and P18 (total dose, 5–7 mg Fe). At P20, Fe concentrations in 4 brain regions (cortex, cerebellum, medulla/pons, and hypothalamus) generally were higher in all groups than in Cu–S pups. At P25, impaired vibrissae-elicited foot placement was evident in Cu–S rats and was not improved by Fe injection. However, at P26, the brain Fe deficit in Cu–S pups was eliminated by Fe injection. Fe injections in Cu– pups raised plasma Fe, brain Fe, and hemoglobin but did not reverse low cytochrome c oxidase or abnormal striatal behavior.