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What Is The Function Of Iron In The Human Body

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Iron: Definition, Function, Importance, Benefits, And Risks

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By Israel C. Nnah Israel C. Nnah Scilit Preprints.org Google Scholar View Publications and Marianne Wessling-Resnick Marianne Wessling-Resnick Scilit Preprints.org Google Scholar View Publications *

Received: 17 October 2018 / Revised: 16 November 2018 / Accepted: 19 November 2018 / Published: 23 November 2018

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Iron is an essential trace element required for important brain functions including oxidative metabolism, synaptic plasticity, myelination, and neurotransmitter synthesis. Many neurodegenerative diseases underlie disruption of brain iron homeostasis. Increasing evidence suggests that brain iron accumulation and chronic neuroinflammation, characterized by microglia activation and secretion of proinflammatory cytokines, are hallmarks of neurodegenerative disorders including Alzheimer’s disease. Although significant efforts have led to an increased understanding of iron metabolism and the role of microglial cells in neuroinflammation, important questions remain unanswered. It remains unclear whether or not increased brain iron contributes to the inflammatory responses of microglial cells, including the molecular cues that guide such responses. How these brain macrophages accumulate, store and use intracellular iron to perform their various functions under normal and disease conditions is not fully understood. Here, we describe the known and emerging mechanisms of microglial cell iron transport and metabolism as well as inflammatory responses in the brain, with a focus on AD.

The brain is among the most metabolically active organs in the body and accounts for at least 20% of the body’s energy consumption. Accordingly, an adequate supply of iron is needed to sustain their high energy needs [1, 2, 3, 4]. Over the past decade our understanding of the role of iron in normal brain function has greatly improved, and much attention has been focused on disentangling the cellular and molecular cues that guide iron transport and metabolism in the brain. These efforts have described the essential roles of iron as a cofactor for several physiological processes including oxidative metabolism, myelination, and the biosynthesis of neurotransmitters [5, 6, 7]. However, excess iron is known to contribute to homeostatic dysregulation due to oxidative stress and is linked to several neurological disorders. Since it is redox active, iron is in both non-ferrous (Fe

) forms and cycles constantly between the two states. Under aerobic conditions, this redox cycling has the potential to generate highly reactive free radicals via Fenton chemistry, leading to oxidative stress and damage to macromolecules. Therefore, the metal is directly related to the disease known as neurodegeneration with the accumulation of brain iron (NBIA), and, in addition to other trace elements related to neurodegeneration, including copper [8], manganese [9], and zinc [10], increasing evidence supports the role of iron in some other sporadic or genetic neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) [11, 12 , 13, 14].

Microglia make up 5 to 12% of the population of cells found in the brain of mice and about 0.5 to 16% of those in the human brain [15, 16]. These resident macrophages are highly involved in immune responses and, depending on the stimuli, can adopt a range of pro- or anti-inflammatory states to help maintain the integrity of the neural environment [17, 18, 19]. In addition to their roles in the neuroinflammatory response, microglia participate in neurogenesis [19, 20], shaping and maintaining synaptic density and connectivity in adults and in the development of the central nervous system (CNS) [16, 21, 22, 23, 24 ], oligodendrocyte differentiation [25], synaptic pruning [26], and myelin repair [16]. Microglia require iron as a cofactor to perform all these different functions [27]. Over the years, multiple studies have reported the roles these immune cells play in brain iron homeostasis [1, 27, 28]. This review will examine the impact of brain iron on microglial metabolism and corresponding inflammatory responses under normal and neurodegenerative conditions, with a particular focus on AD.

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Brain iron levels are tightly regulated to ensure normal CNS function [29, 30]. The major route of iron acquisition begins with intestinal absorption, as does dietary Fe

By duodenal cytochrome B (DcytB) at the apical surface of enterocytes [31]. Divalent metal transporter-1 (DMT1) imports Fe

Into the intestinal cells, and the iron exporter ferroportin (Fpn) makes its way out across this epithelial barrier. On the serosal side, the polycopper ferroxidases oxidize ceruloplasmin and/or hephaestin Fe

, thereby promoting binding to the iron transporter protein transferrin (Tf) [32]. Dietary iron absorption is tightly regulated to respond to the body’s iron needs, so that uptake is enhanced by iron deficiency but reduced under iron loading conditions [29]. Therefore, iron ​​​​​​​​​​​​​​​​​​ that is supplied to the brain from the diet reflects nutritional demands, while at the same time limiting the possibility of excessive accumulation.

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Once in circulation, the entry of iron into the brain from the blood is controlled by the blood-brain barrier (BBB) ​​[33]. The BBB is formed by brain microvascular endothelial cells (BMVECs), pericytes, and astrocytes [33, 34, 35]. Tf-bound iron circulating in the blood outside the CNS cannot directly cross the BBB, and, therefore, iron must enter the brain via BMVECs on a multistep transcellular pathway. The binding of Tf receptors to Tf (TfR) at the lumen of the brain microvasculature facilitates the uptake of iron ​​​​through receptor-mediated endocytosis [30, 34, 36]. The subsequent fate of the Tf-TfR complex within brain endothelial cells is not entirely clear, and how iron is released to the brain remains controversial. The transcytosis model suggests that the ligand-receptor complex crosses the cell, so that Tf is released into the interstitium. However, how Tf could dissociate from its receptor at the abdominal membrane remains unexplained. Another model is that iron is released to the cytoplasm of BMVECs after Tf receptor-mediated endocytosis. The endocytic uptake pathway for iron is much better understood and involves Fe release

, and DMT1-mediated export from the endosome [29]. However, it is unclear whether BMVECs express DMT1 or whether its function is required for iron uptake into the brain, since different groups have reported conflicting data [37, 38, 39, 40, 41, 42]. Another membrane transport mechanism that functions in the release of iron from endolysosomal compartments may involve transient receptor potential mucolipin-1 (TRPML1) channels [43]. A recent study showed that loss of TRPML1 in mice promotes dysregulation of brain homeostasis and reduced myelination, suggesting a possible role in brain iron uptake [44]. Regardless of which carrier is responsible for the release of iron from endocytic compartments, the metal would be used by the endothelial cells for metabolic purposes, stored in endothelial cell ferritin (Ftn), or released to the brain via Fpn [45]. Re-oxidation of Fe

And subsequent incorporation into apo-Tf would provide for its circulation in the brain [46, 47, 48]. It is possible that hepcidin, produced by the brain endothelium, plays a role in the regulation of this process. An in-depth review of iron uptake into BMVECs and its release has been published elsewhere [33].

It is important to note that the amount of Tf in the interstitial fluid of the brain is thought to be much lower than the levels in the systemic circulation, and the levels of non-Tf iron (NTBI) may be quite high [49] . Thus, although Tf appears to be involved in moving iron across the BBB, there is some evidence to suggest that Tf iron-binding sites may become saturated in the brain, so that it is a major source of delivery NTBI is iron to neurons and other cells i. the brain. Another source of iron is ferritin which plays an important role in brain iron homeostasis. Indeed, brain iron dyshomeostasis is the result of genetic loss of ferritin function [11, 50, 51, 52]. The brain may acquire ferritin exogenously through transcellular transport across the BBB, or it may be produced by endothelial cells and released on demand [53]. Other endogenous sources of brain ferritin are possible, including its synthesis by microglia [28]. The ferritin pathway of iron delivery is particularly important for mouse and oligodendrocytes

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