Iron (Fe) deficiency has been reported to be associated with the development of behavioral abnormalities, including impaired learning. Thus, it is reasonable to suggest that a marginal Fe deficiency during development may result in alterations in behavior. Swiss-Webster mice were reared on either control (75 ppm) or marginal Fe (12.5 ppm) diets through pre- and postnatal development. Animals were then subjected to neurobehavioral testing on days 40,50, and 60 postnatal. As tissue copper (Cu) concentrations can increase when there is a reduction in dietary Fe, potentially resulting in an oxidative stress, minerals as well as markers of protein (glutamine synthetase) and lipid oxidation (TBARS) were assessed. Results: Behavioral parameters most significantly affected by the marginal Fe diet were forelimb and hindlimb grip, with the marginal Fe animals exhibiting a 20-55% reduction in strength. Despite 70-90% lower tibia, spleen, and liver Fe levels in the marginal Fe group, there was no evidence of anemia. Brain Fe was somewhat spared, being only 25-30% lower in the caudate, cerebellum, cortex and brainstem relative to controls. This difference in Fe was not sufficient to raise brain Cu levels; furthermore, there was no evidence of protein or lipid oxidation. These data show that a chronic marginal Fe deficiency during critical periods of brain development can result in behavioral abnormalities even in the absence of anemia.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology