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Copper is an essential trace element that is vital to the health of all living things (humans, plants, animals, and microorganisms). In humans, copper is essential to the proper functioning of organs and metabolic processes. The human body has complex homeostatic mechanisms which attempt to ensure a constant supply of available copper, while eliminating excess copper whenever this occurs. However, like all essential elements and nutrients, too much or too little nutritional ingestion of copper can result in a corresponding condition of copper excess or deficiency in the body, each of which has its own unique set of adverse health effects.
Daily dietary standards for copper have been set by various health agencies around the world. Standards adopted by some nations recommend different copper intake levels for adults, pregnant women, infants, and children, corresponding to the varying need for copper during different stages of life.
Copper deficiency and toxicity can be either of genetic or non-genetic origin. The study of copper's genetic diseases, which are the focus of intense international research activity, has shed insight into how human bodies use copper, and why it is important as an essential micronutrient. The studies have also resulted in successful treatments for genetic copper excess conditions, enabling patients whose lives were once jeopardized to live long and productive lives.
Researchers specializing in the fields of microbiology, toxicology, nutrition, and health risk assessments are working together to define the precise copper levels that are required for essentiality, while avoiding deficient or excess copper intakes. Results from these studies are expected to be used to fine-tune governmental dietary recommendation programs which are designed to help protect public health.
|Amine oxidases||Group of enzymes oxidizing primary amines (e.g., tyramine, histidine and polylamines)|
|Ceruloplasmin (ferroxidase I)||Multi-copper oxidase in plasma, essential for iron transport|
|Terminal oxidase enzyme in mitochondrial respiratory chain, involved in electron transport|
|Dopamine β-hydroxylase||Involved in catecholamine metabolism, catalyzes conversion of dopamine to norepinephrine|
|Hephaestin||Multi-copper ferroxidase, involved in iron transport across intestinal mucosa into portal circulation|
|Lysyl oxidase||Cross-linking of collagen and elastin|
|Peptidylglycine alpha-amidating mono-oxygenase (PAM)||Multifunction enzyme involved in maturation and modification of key neuropeptides (e.g., neurotransmitters, neuroendocrine peptides)|
|Superoxide dismutase (Cu, Zn)||Intracellular and extracellular enzyme involved in defense against reactive oxygen species (e.g., destruction of superoxide radicals)|
|Tyrosinase||Enzyme catalyzing melanin and other pigment production|
|Dose range||Approximate daily intakes||Health outcomes|
|Gross dysfunction and disturbance of metabolism of other nutrients; hepatic
"detoxification" and homeostasis overwhelmed
|Toxic||>5.0 mg/kg body weight||Gastrointestinal metallothionein induced (possible differing effects of acute and chronic
|100 μg/kg body weight||Plateau of absorption maintained; homeostatic mechanisms regulate absorption of copper|
|Adequate||34 μg/kg body weight||Hepatic uptake, sequestration and excretion effect homeostasis; glutathione-dependent uptake of copper; binding to metallothionein; and lysosomal excretion of copper|
|11 μg/kg body weight||Biliary excretion and gastrointestinal uptake normal|
|9 μg/kg body weight||Hepatic deposit(s) reduced; conservation of endogenous copper; gastrointestinal
|Deficient||8.5 μg/kg body weight||Negative copper balance|
|5.2 μg/kg body weight||Functional defects, such as lysyl oxidase and superoxide dismutase activities reduced; impaired substrate metabolism|
|2 μg/kg body weight||Peripheral pools disrupted; gross dysfunction and disturbance of metabolism of other
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