Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cu and Fe metabolism are known to be linked, but the interactions during pregnancy are less well studied. In the present study we used rats to examine the effect of Cu deficiency during pregnancy on Fe and Cu levels in maternal and fetal tissue and on the gene expression profile of proteins involved in Cu and Fe metabolism in the placenta. Rats were fed diets with different Cu contents before and during pregnancy. Samples were collected on day 21 of gestation. Cu levels, ceruloplasmin activity and serum Fe all decreased in maternal serum of Cu-deficient animals. Maternal liver Fe inversely correlated with liver Cu. Placental Cu levels decreased with no change in Fe. Fe and Cu levels both decreased in the fetal liver. The drop in maternal liver Cu was significantly correlated with a decrease in organ weight of fetal liver, lung and kidney. No changes were observed in mRNA expression of Cu transporter 1, Menkes P-type Cu-ATPase 7A, Wilson P-type Cu-ATPase 7B, cytochrome-c oxidase, and Cu chaperone Atox1 in the placenta of Cu-deficient dams. Transferrin receptor 1 and the Fe-responsive element (IRE)-regulated divalent metal transporter 1 (DMT1) were up regulated; while ferroportin and non-IRE1-regulated DMT1 levels did not change. These data show that Cu deficiency during pregnancy not only has a direct effect on Fe levels but also regulates the expression of Fe transporters. The pattern closely mirrors that seen in Fe deficiency, suggesting that the changes are a consequence of the decrease in serum Fe, implying that the developing fetus not only suffers from Cu, but also from Fe deficiency.
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PMID:Effect of dietary copper deficiency on iron metabolism in the pregnant rat. 1729 91

The involvement of body copper metabolism in the development of Alzheimer's disease (AD) - the most common form of dementia - is a deeply investigated issue in recent years. Copper is essential for life, but in excess it can be toxic. Recently, it has been hypothesized that copper toxicity may be a contributory factor in the etiology of the neurodegenerative disease AD. Studies on copper evaluation in AD vs. healthy controls collected in the latest 30 years and merged in a meta-analysis demonstrate that serum copper is slightly increased in AD. A specific form of copper, the copper non-bound to ceruloplasmin, or 'free' copper, seems to best characterize this increase in copper in AD patients. Clinical studies from us and other groups have demonstrated that free copper is associated with the typical deficits of AD, incipient AD and mild cognitive impairment, and specific cerebrospinal markers. Moreover, very recent data addressing molecular processes underlying copper dysfunction in AD have indicated that genetic variations of K832R and R952K Single Nucleotide Polymorphisms (SNPs) of the Wilson's disease gene ATP7B are associated also with sporadic AD. Specifically, ATP7B encodes for the protein ATPase 7B which controls free copper status in the body, and both R allele in K832R and K allele in R952K ATP7B SNPs are associated with an increased risk of having AD. Even though copper dysfunction cannot be assumed as a determinant of the disease, its causative, rather than associated, role in AD pathology as risk factor can be claimed.
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PMID:Copper dysfunction in Alzheimer's disease: from meta-analysis of biochemical studies to new insight into genetics. 2256 15