LiveingWell Health News Letter
1.COPPER 2. HEALTH SITES 3.IN THE NEWS: THOUGHT OF THE DAY
Copper (Cu) is an essential trace element for humans and animals. In the body, copper shifts between the cuprous (Cu1+) and the cupric (Cu2+) forms, though 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. Although Hippocrates is said to have prescribed copper compounds to treat diseases as early as 400 B.C., scientists are still uncovering new information regarding the functions of copper in the human body.
Copper is a critical functional component of a number of essential enzymes, known as cuproenzymes. Some of the physiologic functions known to be copper-dependent are discussed below.
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 maintain the integrity of connective tissue in the heart and blood vessels and plays a role in bone formation.
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.
Metabolism of neurotransmitters: Monoamine oxidase (MAO) plays a role in the metabolism of the neurotransmitters norepinephrine, epinephrine, 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 is made of phospholipids whose synthesis depends on cytochrome c oxidase activity.
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: Ceruloplasmin may function as an antioxidant in two different ways. Free copper and iron ions are powerful catalysts of free radical damage. By binding copper, ceruloplasmin prevents free copper ions from catalyzing oxidative damage. The ferroxidase activity of ceruloplasmin (oxidation of ferrous iron) facilitates iron loading onto its transport protein, transferrin, and may prevent free ferrous ions (Fe2+) from participating in harmful free radical generating reactions.
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.
Iron: Adequate copper nutritional status appears to be necessary for normal iron metabolism and red blood cell formation. Anemia 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 (see Iron Metabolism). Infants fed a high iron formula absorbed less copper than infants fed a low iron formula, suggesting that high iron intakes may interfere with copper absorption in infants.
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.
Fructose: High fructose diets have exacerbated copper deficiency in rats, but not in pigs whose gastrointestinal systems are more like those of humans. Very high levels of dietary fructose (20% of total calories) did not result in copper depletion in humans, suggesting that fructose intake does not result in copper depletion at levels relevant to normal diets.
Vitamin C: Although vitamin C supplements have produced copper deficiency in laboratory animals, the effect of vitamin C supplements on copper nutritional status in humans is less clear. Two small studies in healthy young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C. In one study, vitamin C supplementation of 1,500 mg/day for 2 months resulted in a significant decline in ceruloplasmin oxidase activity. In the other study, supplements of 605 mg of vitamin C/day for 3 weeks resulted in decreased ceruloplasmin oxidase activity, although copper absorption did not decline. Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status.
Clinically evident or frank 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 anemia that is unresponsive to iron therapy but corrected by copper supplementation. The anemia is thought to result from defective iron mobilization due to decreased ceruloplasmin activity. Copper deficiency may also result in abnormally low numbers of white blood cells known as neutrophils (neutropenia), 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. Less common features of copper deficiency may include loss of pigmentation, neurological symptoms, and impaired growth.
Individuals at risk of deficiency
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. High-risk individuals include: premature infants, especially those with low-birth weight, infants with prolonged diarrhea, infants and children recovering from malnutrition, individuals with malabsorption syndromes, including celiac disease, sprue, and short bowel syndrome due to surgical removal of a large portion of the intestine. Individuals receiving intravenous total parenteral nutrition or other restricted diets may also require supplementation with copper and other trace elements. Recent research indicates that cystic fibrosis patients may also be at increased risk of copper insufficiency.
By Lillian Waugh
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