The Effects of Early Iron Deficiency on Brain Iron and Monoamine Levels in a Rat Model

Open Access
Fassihi, Safa Cyrus
Area of Honors:
Bachelor of Science
Document Type:
Thesis Supervisors:
  • Dr Erica Unger, Thesis Supervisor
  • Bernhard Luscher, Honors Advisor
  • Dr Gong Chen, Faculty Reader
  • Iron
  • Deficiency
  • Rats
  • Brain
  • Monoamine
  • Neurotransmitter
The purpose of the thesis project is to examine the long-term effects of gestational and early lactational iron deficiency on brain iron and monoamine levels in a rat model of early iron deficiencies. There is existing evidence that early iron deficiency can significantly alter primary functions of rats that persist into adulthood (i.e. altered sensorimotor development and brain monoamines) even after iron supplementation at weaning (postnatal day (P) 21). Thus, the current study focuses on determining whether earlier iron repletion at P8 can prevent the long-term neurochemical outcomes associated with early iron deficiency. Assuming a 22 day gestation period, neurodevelopment of rats at P8 is the equivalent of birth in humans. In this study, rats were subjected to one of three dietary treatments: 1) iron sufficient through gestation and lactation; 2) iron deficient beginning on gestational day 5 (G5) and continuing through lactation; and 3) iron deficient beginning on G5 followed by moderate iron treatment beginning on P8. The results, attained via batch average and ANOVA, suggest that early iron deficiency in rats reduces brain iron in various regions (p<0.05), alters hematological markers of iron status (p<0.05), and has no significant effect (p>0.05) on brain monoamines and metabolites. Furthermore, moderate-dosed iron therapy at P8 corrects for iron deficits in the brain and blood at P21 and P90. Therefore, these findings suggest that P8 is a suitable age for iron-therapy to begin with respect to normalization of iron concentrations and the associated hematological markers.