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Articles

Chronic Marginal Iron Intakes during Early Development in Mice Result in Persistent Changes in Dopamine Metabolism and Myelin Composition¹

Catherine L. Kwik-Uribe^*, Dorothy Gietzen, J. Bruce German^**, Mari S. Golub and Carl L. Keen^*2

Departments of ^* Nutrition, Anatomy, Physiology and Cell Biology (Veterinary Medicine), ^** Food Science & Technology and Internal Medicine, University of California, Davis, CA 95616

²To whom correspondence and reprint requests should be addressed.

Marginal iron (Fe) deficiency is prevalent in children worldwide, yet the behavioral and biochemical effects of chronic marginal Fe intakes during early development are not well characterized. Using a murine model, previous work in our laboratory demonstrated persistent behavioral disturbances as a consequence of marginal Fe intakes during early development. In the present study, Swiss-Webster mice fed a control Fe diet (75 µg Fe/g diet, n = 13 litters) or marginal Fe diet (14 µg Fe/g diet, n = 16 litters) during gestation and through postnatal day (PND) 75 were killed on PND 75 for assessment of tissue mineral concentrations, dopamine metabolism, myelin fatty acid composition, and c- and m-aconitase activities. In addition, these outcomes were assessed in a group of offspring (n = 13 litters) fed a marginal Fe diet during gestation and lactation and then fed a control diet from PND 21–75. Marginal Fe mice demonstrated significant differences in brain iron concentrations, dopamine metabolism and myelin fatty acid composition relative to control mice; however, no difference in c- or m-aconitase activity was demonstrated in the brain. The postnatal consumption of Fe-adequate diets among marginal Fe offspring did not fully reverse all of the observed biochemical disturbances. This study demonstrates that chronic marginal Fe intakes during early development can result in significant changes in brain biochemistry. The persistence of some of these biochemical changes after postnatal Fe supplementation suggests that they are an irreversible consequence of developmental Fe restriction.

KEY WORDS: • iron deficiency • marginal iron • dopamine • myelin • c-aconitase • m-aconitase • mice

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