Food-Info.net > Minerals

Copper (Cu)

• Introduction
• Food Sources
• Recommended Dietary Allowance
• Inhibitors/Stimulators
• Functions in the body
• Deficiency
• Toxicity
• Regulation
• Questions and Answers
• Sources

 

Introduction

Copper is an essential trace element for humans and animals. In the body, copper shifts between the cuprous (Cu¹⁺) and the cupric (Cu²⁺) forms although the majority of the body's copper is in the Cu²⁺ form. The ability of copper to easily accept and donate electrons explains its important role in oxidation-reduction (redox) reactions and the scavenging of free radicals. Scientists are still uncovering new information regarding the functions of copper in the human body.

 

Food Sources

Copper is found in a wide variety of foods and is most plentiful in organ meats, shellfish, nuts, and seeds. Wheat bran cereals and whole grain products are also good sources of copper. The concentrations in plant sources may vary from place to place because soil mineral content varies geographically.

Some important food sources of copper:

 

Liver	Oysters	Sardines	Sunflower seeds	Crab
Lobster	Peanuts	Mushrooms	Dried Plums	Almonds

 

Recommended Dietary Allowance (RDA)

The European Union RDA for the general population is set at 1,15 mg/day.

The RDA for copper reflects the results of depletion-repletion studies and is based on the prevention of deficiency.

 

Inhibitors/stimulators:

The following food components have been found to stimulate the absorption of copper:

 

Iron � Adequate copper nutritional status appears to be necessary for normal iron metabolism and red blood cell formation. Anaemia is a clinical sign of copper deficiency, and iron has been found to accumulate in the livers of copper deficient animals, indicating that copper (probably in the form of ceruloplasmin) is required for iron transport to the bone marrow for red blood cell formation.

 

The following food components have been found to inhibit the absorption of copper:

 

Zinc � High supplemental zinc intakes of 50 mg/day or more for extended periods of time may result in copper deficiency. High dietary zinc increases the synthesis of an intestinal cell protein called metallothionein, which binds certain metals and prevents their absorption by trapping them in intestinal cells. Metallothionein has a stronger affinity for copper than zinc, so high levels of metallothionein induced by excess zinc cause a decrease in intestinal copper absorption. High copper intakes have not been found to affect zinc nutritional status.

 

Molybdenum � Molybdenum is an antagonist to copper absorption.

 

Functions in the Body

Copper is a critical functional component of a number of essential enzymes, known as cuproenzymes. Some of the physiological functions known to be copper-dependent are discussed below.

Energy production
The copper-dependent enzyme, cytochrome c oxidase, plays a critical role in cellular energy production. By catalyzing the reduction of molecular oxygen (O₂) to water (H₂O), cytochrome c oxidase generates an electrical gradient used by the mitochondria to create the vital energy-storing molecule, ATP.

Connective tissue formation
Another cuproenzyme, lysyl oxidase, is required for the cross-linking of collagen and elastin, which are essential for the formation of strong and flexible connective tissue. The action of lysyl oxidase helps to maintain the integrity of connective tissue in the heart and blood vessels and plays a role in bone formation.

Iron metabolism
Two copper-containing enzymes, ceruloplasmin (ferroxidase I) and ferroxidase II have the capacity to oxidize ferrous iron (Fe²⁺) to ferric iron (Fe³⁺), the form of iron that can be loaded onto the protein transferrin for transport to the site of red blood cell formation. Although the ferroxidase activity of these two cuproenzymes has not yet been proven to be physiologically significant, the fact that iron mobilization from storage sites is impaired in copper deficiency supports their role in iron metabolism.

Central nervous system
A number of reactions essential to normal function of the brain and nervous system are catalyzed by cuproenzymes.

Neurotransmitter synthesis
Dopamine-b-monooxygenase catalyzes the conversion of dopamine to the neurotransmitter norepinephrine (noradrenalin).

Metabolism of neurotransmitters
Monoamine oxidase (MAO) plays a role in the metabolism of the neurotransmitters norepinephrine, epinephrine (adrenalin), and dopamine. MAO also functions in the degradation of the neurotransmitter serotonin, which is the basis for the use of MAO inhibitors as antidepressants.

Formation and maintenance of myelin
The myelin sheath (cell wall of nerve cells) is made of phospholipids whose synthesis depends on cytochrome c oxidase activity.

Melanin formation
The cuproenzyme tyrosinase, is required for the formation of the pigment melanin. Melanin is formed in cells called melanocytes and plays a role in the pigmentation of the hair, skin, and eyes.

Superoxide dismutase
Superoxide dismutase (SOD) functions as an antioxidant by catalyzing the conversion of superoxide radicals (free radicals or ROS) to hydrogen peroxide, which can subsequently be reduced to water by other antioxidant enzymes. Two forms of SOD contain copper: 1) copper/zinc SOD is found within most cells of the body, including red blood cells, and 2) extracellular SOD is a copper containing enzyme found in high levels in the lungs and low levels in blood plasma.

Ceruloplasmin
The cupper containing protein ceruloplasmin functions as an antioxidant in blood serum .

Regulation of gene expression
Copper-dependent transcription factors regulate transcription of specific genes. Thus, cellular copper levels may affect the synthesis of proteins by enhancing or inhibiting the transcription of specific genes. Genes regulated by copper-dependent transcription factors include genes for copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (another antioxidant enzyme), and proteins related to the cellular storage of copper.

 

Deficiency

Clinically evident copper deficiency is relatively uncommon. Serum copper levels and ceruloplasmin levels may fall to 30% of normal in cases of severe copper deficiency. One of the most common clinical signs of copper deficiency is an anaemia that is unresponsive to iron therapy but corrected by copper supplementation. Copper deficiency may also result in abnormally low numbers of white blood cells known as neutrophils (neutropaenia), a condition that may be accompanied by increased susceptibility to infection. Osteoporosis and other abnormalities of bone development related to copper deficiency are most common in copper-deficient low-birth weight infants and young children.

Cow's milk is relatively low in copper, and cases of copper deficiency have been reported in high-risk infants and children fed only cow's milk formula.

Toxicity

Copper toxicity is rare in the general population. Symptoms of acute copper toxicity include abdominal pain, nausea, vomiting, and diarrhoea, which help to prevent additional ingestion and absorption of copper. More serious signs of acute copper toxicity include severe liver damage, kidney failure, coma, and death. Of more concern from a nutritional standpoint is the possibility of liver damage resulting from long-term exposure to lower doses of copper.

In general, healthy individuals, doses of up to 10,000 µg (10 mg) daily have not resulted in liver damage. It should be noted that individuals with genetic disorders affecting copper metabolism (Wilson's disease, Indian childhood cirrhosis, and idiopathic copper toxicosis) may be at risk of adverse effects of chronic copper toxicity at significantly lower intake levels.

Regulation

Copper can enter the body during drinking or eating substances that contain copper. Copper can also enter the body through breathing air or dust containing copper. Copper may enter the lungs of workers exposed to copper dust or fumes.

Copper rapidly enters the bloodstream and is distributed throughout the body after one eats or drinks it. Certain substances in foods eaten with copper can affect the amount of copper that enters the bloodstream from the gastrointestinal tract. The body is very good at blocking high levels of copper from entering the bloodstream. It's unknown as to how much copper enters the body through the lungs or skin. Copper then leaves the body in faeces and urine, mostly in faeces. It takes several days for copper to leave the body. Generally, the amount of copper in the body remains constant (the amount that enters your body equals the amount that leaves).

QA on Copper

Sources :

Ursel, A. : Natural care � Vitamins & Minerals Handbook. Dorling Kindersley, London, 2001. ISBN 80-89179-01-0

Dutch Nutrition Centre : www.voedingscentrum.nl/

http://dietary-supplements.info.nih.gov/Health_Information/Vitamin_and_Mineral_Supplement_Fact_Sheets.aspx

Images adapted from here.

www.atsdr.cdc.gov/toxprofiles/