Abstract
Copper, which can potentially be a highly toxic agent, is an essential nutrient due to its role as a cofactor for cuproenzymes and its participation in signaling pathways. In mammals, the liver is a central organ that controls copper turnover throughout the body, including copper absorption, distribution, and excretion. In ontogenesis, there are two types of copper metabolism, embryonic and adult, which maintain the balance of copper in each of these periods of life, respectively. In the liver cells, these types of metabolism are characterized by the specific expression patterns and activity levels of the genes encoding ceruloplasmin, which is the main extracellular ferroxidase and copper transporter, and the proteins mediating ceruloplasmin metalation. In newborns, the molecular genetic mechanisms responsible for copper homeostasis and the ontogenetic switch from embryonic to adult copper metabolism are highly adapted to milk ceruloplasmin as a dietary source of copper. In the mammary gland cells, the level of ceruloplasmin gene expression and the alternative splicing of its pre-mRNA govern the amount of ceruloplasmin in the milk, and thus, the amount of copper absorbed by a newborn is controlled. In newborns, the absorption, distribution, and accumulation of copper are adapted to milk ceruloplasmin. If newborns are not breast-fed in the early stages of postnatal development, they do not have this natural control ensuring alimentary copper balance in the body. Although there is still much to be learned about the neonatal consequences of having an imbalance of copper in the mother/newborn system, the time to pay attention to this problem has arrived because the neonatal misbalance of copper may provoke the development of copper-related disorders.
Highlights
A suboptimal content of micronutrients in a mother’s diet during pregnancy and lactation may be a cause of developmental defects in newborns
The reviewed data suggest that the copper imbalance in the early postnatal period, which is induced by feeding infants formula, influences various aspects of copper metabolism
This is primarily an increase in the Cp and copper concentrations in the blood serum and cerebrospinal fluid, but there is no evidence that it can affect the formation of cuproenzymes
Summary
A suboptimal content of micronutrients in a mother’s diet during pregnancy and lactation may be a cause of developmental defects in newborns. The liver and the brain, the organs with the most intensive copper metabolism [19], are affected first by the defects of copper transport. In these organs, signs of toxic copper accumulation and cuproenzyme deficiency manifest earlier than in other organs. Dietary factors may cause copper misbalance in the early stages of postnatal development. Copper deficiency in the food of pregnant and nursing females causes a lack of cuproenzyme activity, multiple developmental aberrations, teratoma formation, and death among fetuses or offspring in the early postnatal stages [21,22]. The aims of the present review are to emphasize the dependence of copper homeostasis in newborns on food sources and to pay attention to the possible long-term consequences of copper imbalances in neonates
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