Association between Serum Copper Status and Working Memory in Schoolchildren

Zhou, Guoping; Ji, Xiaopeng; Cui, Naixue; Cao, Sanxing; Liu, Chang; Liu, Jianghong

doi:10.3390/nu7095331

Cited by 40 publications

(21 citation statements)

References 27 publications

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“…Consistent with our results, a recent study has reported a significant association between high copper levels in blood and poorer cognitive performance in normal school children (Zhou et al. ).…”

Section: Discussionsupporting

confidence: 93%

Airborne copper exposure in school environments associated with poorer motor performance and altered basal ganglia

et al. 2016

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IntroductionChildren are more vulnerable to the effects of environmental elements. A variety of air pollutants are among the identified factors causing neural damage at toxic concentrations. It is not obvious, however, to what extent the tolerated high levels of air pollutants are able to alter brain development. We have specifically investigated the neurotoxic effects of airborne copper exposure in school environments.MethodsSpeed and consistency of motor response were assessed in 2836 children aged from 8 to 12 years. Anatomical MRI, diffusion tensor imaging, and functional MRI were used to directly test the brain repercussions in a subgroup of 263 children.ResultsHigher copper exposure was associated with poorer motor performance and altered structure of the basal ganglia. Specifically, the architecture of the caudate nucleus region was less complete in terms of both tissue composition and neural track water diffusion. Functional MRI consistently showed a reciprocal connectivity reduction between the caudate nucleus and the frontal cortex. ConclusionsThe results establish an association between environmental copper exposure in children and alterations of basal ganglia structure and function.

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Section: Discussionsupporting

confidence: 93%

Airborne copper exposure in school environments associated with poorer motor performance and altered basal ganglia

et al. 2016

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“…Such effects can be very significant, but now their identification is difficult. Because some participants of the CTS are still unknown while some copper-binding proteins are ‘moonlighting’ and their activities depend on the copper level (e.g., Cp, CTR1, ATOX1, and COMMD1) [ 36 , 167 , 168 , 169 , 170 , 171 ], we may suggest that the differences between breastmilk and infant formula with respect to copper concentrations and copper ‘packaging’ by the Cp protein may be one of the factors that contribute to the negative effects of bottle feeding on the cognitive abilities of children [ 172 , 173 ].…”

Section: Resultsmentioning

confidence: 99%

Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin as a Nutritive Source of Copper: Overview of the Current Data

et al. 2018

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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.

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“…Because some participants of CTS are still unknown while some copper-binding proteins are 'moonlighting' and their activities dependent on copper level (e.g. Cp, CTR1, ATOX1, COMMD1) [31,[151][152][153][154][155], we may suggest that the differences between breastmilk and infant formulas with respect to copper concentrations and copper 'packaging' by the Cp protein may be one of the factors that contribute to the negative effects of bottle feeding on the cognitive abilities of children [156,157].…”

Section: Resultsmentioning

confidence: 99%

Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin As a Nutritive Source of Copper

Puchkova¹,

Babich²,

Zatulovskaia³

et al. 2018

Preprint

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Copper, which can potentially be a highly toxic agent, is an essential nutrient due to its role as a co-factor for cuproenzymes and participation in signaling pathways. In mammals, the liver is a central organ that controls copper turnover throughout the body: 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, respectively. In the liver cells, these types are characterized by specific expression patterns and activity levels of the genes encoding ceruloplasmin, which is the main extracellular ferroxidase and copper transporter and 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 milk, and thus, the amount of copper absorbed by the newborn is controlled. In the newborns, absorption, distribution, and accumulation copper are adapted to milk ceruloplasmin. In the newborns, which are not breast-fed at the early stages of postnatal development, the control for alimentary copper balance is absent. We tried to focus on the neonatal consequences of a violation of the balance of copper in the mother / newborn system. Although there is still much to be learned, the time to pay attention to this problem came because the neonatal misbalance of copper may provoke the development of copper related disorders for future life.

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Association between Serum Copper Status and Working Memory in Schoolchildren

Cited by 40 publications

References 27 publications

Airborne copper exposure in school environments associated with poorer motor performance and altered basal ganglia

Airborne copper exposure in school environments associated with poorer motor performance and altered basal ganglia

Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin as a Nutritive Source of Copper: Overview of the Current Data

Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin As a Nutritive Source of Copper

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