Abstract
Iron is an essential nutrient during all stages of mammalian development. Studies carried out over the last 20 years have provided important insights into cellular and systemic iron metabolism in adult organisms and led to the deciphering of many molecular details of its regulation. However, our knowledge of iron handling in prenatal development has remained remarkably under-appreciated, even though it is critical for the health of both the embryo/fetus and its mother, and has a far-reaching impact in postnatal life. Prenatal development requires a continuous, albeit quantitatively matched with the stage of development, supply of iron to support rapid cell division during embryogenesis in order to meet iron needs for erythropoiesis and to build up hepatic iron stores, (which are the major source of this microelement for the neonate). Here, we provide a concise overview of current knowledge of the role of iron metabolism-related genes in the maintenance of iron homeostasis in pre- and post-implantation development based on studies on transgenic (mainly knock-out) mouse models. Most studies on mice with globally deleted genes do not conclude whether underlying in utero iron disorders or lethality is due to defective placental iron transport or iron misregulation in the embryo/fetus proper (or due to both). Therefore, there is a need of animal models with tissue specific targeted deletion of genes to advance the understanding of prenatal iron metabolism.
Highlights
Iron is an essential redox element that functions as a cofactor of many hemo- and iron-sulfur [Fe-S] proteins required to sustain fundamental life processes including DNA synthesis and repair, ATP production, cell cycle, oxygen transport, and detoxification
There are still many more questions to answer about the regulation of iron homeostasis in prenatal life
In order to fully understand prenatal iron balance, it is crucial to distinguish between the mechanism and regulation of iron transport across the placenta, between maternal and fetal regulation and between embryo proper vs. extraembryonic structures
Summary
Iron is an essential redox element that functions as a cofactor of many hemo- and iron-sulfur [Fe-S] proteins required to sustain fundamental life processes including DNA synthesis and repair, ATP production, cell cycle, oxygen transport, and detoxification. Considering that the redox activity of iron can generate, through the Fenton reaction, hydroxyl free radicals capable of causing a wide range of biological damage [3], the second challenge of iron homeostasis is minimizing its toxicity This dual homeostatic assignment is achieved via the functioning of a complex protein machinery involving transmembrane iron transporters, chaperones, iron storage proteins, ferrireductases, and ferroxidases. In contrast to well-defined pathways of intestinal absorption of exogenous iron operating postnatally, in prenatal life, iron reaches to the organism through the transfer across at first the visceral endoderm (VE), structures called “early placenta” [8] and fully developed/specialized placenta This process is the subject of a complex, regulatory interplay among the mother, fetus, and the placenta itself (reviewed in [10]). At E7.5 and E8.5 embryos start to be resorbed and reduced to a small mass of embryonic tissue surrounded by maternal hemmorrhagic tissue Complete resorption at E9.5
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