Main article: Copper in health
Rich sources of copper include oysters, beef and lamb liver, Brazil nuts, blackstrap molasses, cocoa, and black pepper. Good sources include lobster, nuts and sunflower seeds, green olives, avocados, and wheat bran.
Copper proteins have diverse roles in biological electron transport and oxygen transportation, processes that exploit the easy interconversion of Cu(I) and Cu(II).The biological role for copper commenced with the appearance of oxygen in earth's atmosphere. The protein hemocyanin is the oxygen carrier in most mollusks and some arthropods such as the horseshoe crab(Limulus polyphemus) Because hemocyanin is blue, these organisms have blue blood, not the red blood found in organisms that rely on hemoglobin for this purpose. Structurally related to hemocyanin are the laccases and tyrosinases. Instead of reversibly binding oxygen, these proteins hydroxylate substrates, illustrated by their role in the formation of lacquers.
Copper is also a component of other proteins associated with the processing of oxygen. In cytochrome c oxidase, which is required for aerobic respiration, copper and iron cooperate in the reduction of oxygen. Copper is also found in many superoxide dismutases, proteins that catalyze the decomposition of superoxides, by converting it (by disproportionation) to oxygen and hydrogen peroxide:
Several copper proteins, such as the "blue copper proteins", do not interact directly with substrates, hence they are not enzymes. These proteins relay electrons by the process called electron transfer.
A unique tetranuclear copper center has been found in nitrous-oxide reductase.
Copper is an essential trace element in plants and animals, but not some microorganisms. The human body contains copper at a level of about 1.4 to 2.1 mg per kg of body mass. Stated differently, the RDA for copper in normal healthy adults is quoted as 0.97 mg/day and as 3.0 mg/day. Copper is absorbed in the gut, then transported to the liver bound to albumin. After processing in the liver, copper is distributed to other tissues in a second phase. Copper transport here involves the protein ceruloplasmin, which carries the majority of copper in blood. Ceruloplasmin also carries copper that is excreted in milk, and is particularly well-absorbed as a copper source.Copper in the body normally undergoes enterohepatic circulation (about 5 mg a day, vs. about 1 mg per day absorbed in the diet and excreted from the body), and the body is able to excrete some excess copper, if needed, via bile, which carries some copper out of the liver that is not then reabsorbed by the intestine.
Because of its role in facilitating iron uptake, copper deficiency can produceanemia-like symptoms, neutropenia, bone abnormalities, hypopigmentation, impaired growth, increased incidence of infections, osteoporosis, hyperthyroidism, and abnormalities in glucose and cholesterol metabolism. Conversely, Wilson's disease causes an accumulation of copper in body tissues.
Severe deficiency can be found by testing for low plasma or serum copper levels, low ceruloplasmin, and low red blood cell superoxide dismutase levels; these are not sensitive to marginal copper status. The "cytochrome c oxidase activity of leucocytes and platelets" has been stated as another factor in deficiency, but the results have not been confirmed by replication.
Main article: Copper toxicity
Gram quantities of various copper salts have been taken in suicide attempts and produced acute copper toxicity in humans, possibly due to redox cycling and the generation of reactive oxygen species that damage DNA. Corresponding amounts of copper salts (30 mg/kg) are toxic in animals. A minimum dietary value for healthy growth in rabbits has been reported to be at least 3 ppm in the diet. However, higher concentrations of copper (100 ppm, 200 ppm, or 500 ppm) in the diet of rabbits may favorably influence feed conversion efficiency, growth rates, and carcass dressing percentages.
Chronic copper toxicity does not normally occur in humans because of transport systems that regulate absorption and excretion. Autosomal recessive mutations in copper transport proteins can disable these systems, leading to Wilson's disease with copper accumulation and cirrhosis of the liver in persons who have inherited two defective genes.
Elevated copper levels have also been linked to worsening symptoms ofAlzheimer's disease.