Abstract

The transition metal iron exerts essential roles in the central nervous system (CNS) for oxygen transport, myelin formation, and synthesis of neurotransmitters. Being redox active, iron switches between ferrous and ferric states. Switching between oxygen states also makes iron an important inducer of reactive oxygen species through the Fenton and Haber-Weiss reactions. Such reactive oxygen species are potentially damaging to nucleic acids, proteins, and fatty acids, which makes the handling of iron very important. Both of iron overload and iron deficiency are detrimental to cells of the nervous system. Iron overload increases the formation of oxidative species and thereby increasing risks for neuronal death, and regional iron accumulation in the brain is associated with neurodegenerative disorders like Alzheimer's disease and Parkinson's disease (Rouault, 2013; Andersen et al., 2014; Ward et al., 2014). Systemic iron overloading causes hemochromatosis with the surprising absence of brain impairment, which is attributed to down-regulation of the iron uptake and transport at the blood-brain barrier (BBB) (Andersen et al., 2014). Conversely, limited access to iron leads to systemic iron deficiency that may affect the iron levels in the CNS and peripheral nervous system, which can cause cell growth arrest or even cell death. This suggests that maternal iron deficiency seriously can affect the developing foetus, including the brain.

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