Copper (63,5 a.m.u.) present in two conditions in human body – Cu2+ and Cu1+; easy transformation ensures its oxidizing-recovering properties. Copper creates a stable bond with proteins, peptides and other organic elements, concentration of free copper in cytoplasm is very low. Key organ in copper metabolism is liver – content of copper-containing enzymes and other proteins. More than 90% of copper is being transported from liver to peripheral tissues in complex with caeruloplasmin.
Copper is a catalytic component of several enzymes and structural element of many vital proteins. Most part of multiple copper-containing proteins are oxidases, localizing outside cytoplasm on the surface of cell membranes or in vesicles. Copper-containing metal-enzyme – superoxide dismutase – provides protection for plasm and cytoplasm components from free radicals. Cytochrome-c-oxidase enzyme is important for intercellular processes. Lysyl oxidase is vital for stabilization of extracellular matrix, including development of cross-bonds of collagen and elastin. Copper-containing enzymes, including caeruloplasmin are present in iron metabolism. Copper-containing enzyme, catalysing dopamine transformation to noradrenalin is also an enzyme, catalysing melatonin synthesis. Copper-containing proteins are a part of gene transcription processes.
Content of copper in food products is variable and depends on the food cooking conditions and supplements. Meat products contains a lot of copper, quite a lot – in sea products, nuts, whole grains, boltings and cocoa-containing products. Milk products (goat milk) and white meat contains very low concentrations of copper.
Inborn copper metabolism defects cause heavy disorders: Menkes syndrome (genetic disorder of copper absorption in intestinal canal), Wilson’s disease (disorder of copper transportation, including its involvement in caeruloplasmin, combined with aggregation of copper in organs and tissues). Copper deficiency symptoms include neutropenia, anaemia (resistant to iron medicines), osteoporosis, neurologic symptoms and heartbeat disorders. Copper absorption deficit could be indicated in diffuse diseases of small intestine together with high concentration of competing zinc and cadmium ions. Copper deficit could be reported for nursing infants (especially – premature children), patients receiving long-lasting parenteral feeding with micronutrients deficiency, taking zinc-type drugs, like penicillamine.
Symptoms of copper salts intoxication (fungicide activities, absorption of copper-containing solutions) are indicating sickness, vomit, headache, diarrhoea, stomach pain. In cases of copper intoxication liver diseases, hepatitis and hemocidal shock are possible. To evaluate copper status, it would be recommended to establish copper concentration level in plasm together with establishment of caeruloplasmin level, however, in cases of allied changes these investigations could not be sensible enough.
