Strong interest in copper homeostasis is due to the fact that copper is simultaneously a catalytic co-factor of the vital enzymes, a participant in signaling, and a toxic agent provoking oxidative stress. In mammals, during development copper metabolism is conformed to two types. In embryonic type copper metabolism (ETCM), newborns accumulate copper to high level in the liver because its excret...

Copper is a redox active metal that is essential for biological function. Copper is potentially toxic; thus, its homeostasis is carefully regulated through a system of protein transporters. Copper is taken up across the lumen surface of the small intestinal microvilli as cuprous ion by Ctr1. Cupric ion may also be taken up, but those processes are less well understood. Within the cell, intestin...

Copper is an essential micronutrient for cell growth but is toxic in excess. Copper transporter (Ctr1) plays an important role in regulating adequate copper levels in mammalian cells. We have shown previously that expression of the human high-affinity copper transporter (hCtr1) was transcriptionally up-regulated under copper-depleted conditions and down-regulated under replete conditions; moreo...

the relationship between different indices of the copper deficiency was studied in 136 slaughtered male cattle (< 2 years). copper status has been detected as marginally deficient in 57.4, 36.4, 34.6, and 28.2% of cattle based on the copper concentrations in plasma (5.5-14.5 μmol/l) and liver (19.7-189.1 mg/kgdm), plasma ceruloplasmin levels (85.4 - 178.2 mg/l) and erythrocyte superoxide dismut...

Body copper homeostasis is regulated by the liver, which removes excess copper via bile. In Wilson's disease (WD), this function is disrupted due to inactivation of the copper transporter ATP7B resulting in hepatic copper overload. High urinary copper is a diagnostic feature of WD linked to liver malfunction; the mechanism behind urinary copper elevation is not fully understood. Using Positron ...

BACKGROUND Genetic and environmental factors, including dietary copper intake, contribute to the pathogenesis of copper-associated hepatitis in Labrador retrievers. Clinical disease is preceded by a subclinical phase in which copper accumulates in the liver. OBJECTIVE To investigate the effect of a low-copper, high-zinc diet on hepatic copper concentration in Labrador retrievers with increase...

An abnormal copper metabolism can cause hepatic copper accumulation and subsequently an increase in oxidative stress. We therefore analyzed the copper metabolism pathways and (non)enzymatic defenses against ROS in three different forms of chronic liver failure in the dog. Chronic hepatitis caused by inherited copper toxicosis (Copper toxicosis, CT) was compared to chronic hepatitis of unknown e...

Copper is an essential trace element in many organisms and is utilized in all domains of life. It is often used as a cofactor of redox proteins, but is also a toxic metal ion. Intracellular copper must be carefully handled to prevent the formation of reactive oxygen species which pose a threat to DNA, lipids, and proteins. In this work, we examined patterns of copper utilization in prokaryotes ...

OBJECT Anemia and leukopenia caused by copper deficiency are well-documented consequences of long-term total parenteral nutrition. We measured the serum copper levels of bed-ridden patients receiving enteral feeding, and evaluated optical and ultrastructural features of bone marrow before and after copper supplementation. PATIENTS AND METHODS Serum samples were obtained from 15 bed-ridden eld...

Over the past two decades there have been significant advances in our understanding of copper homeostasis and the pathological consequences of copper dysregulation. Cumulative evidence is revealing a complex regulatory network of proteins and pathways that maintain copper homeostasis. The recognition of copper dysregulation as a key pathological feature in prominent neurodegenerative disorders ...