Copper (intracellular)

A cofactor for connective tissue (lysyl oxidase), iron transport (caeruloplasmin), mitochondria (cytochrome c oxidase) and the formation of noradrenaline from dopamine (DBH). The ratio of copper to zinc is looked at in questions of inflammation.

What copper does in the cell

Copper enters the cells via the transporter CTR1 after it has been converted into the monovalent form at the cell surface. It is practically never free inside the cell, because free copper would generate reactive oxygen species. Instead, escort proteins, the copper chaperones, take care of distribution: CCS brings copper to superoxide dismutase in the cytoplasm, COX17 to cytochrome c oxidase in the mitochondria, and ATOX1 to the copper pumps ATP7A and ATP7B. In the Golgi apparatus these load enzymes such as lysyl oxidase for connective tissue, tyrosinase for the skin pigment melanin and dopamine β-hydroxylase for noradrenaline; in the liver, ATP7B passes excess copper into the bile. Inside the cell, copper is stored and buffered on metallothionein and glutathione.

Low copper in the cell – what happens in the body?

When copper is lacking in the cell, the copper-dependent enzymes remain partly unloaded. Superoxide dismutase defuses less superoxide, cytochrome c oxidase at the end of the respiratory chain works more slowly, and the cell gains less ATP. Tyrosinase forms less melanin, which can show as lighter pigmentation of the skin and hair, and lysyl oxidase cross-links collagen and elastin more weakly. These bottlenecks are particularly noticeable in blood-forming cells and nerve cells. Causes are very high zinc intake, in which the gut cells bind copper to metallothionein and do not pass it on, impaired absorption in the gut and the rare inherited Menkes disease, in which the ATP7A pump is missing.

High copper in the cell – what happens in the body?

When the copper content of the cells rises, the stores on metallothionein and glutathione fill up first. When these buffers are exceeded, unbound copper is produced, which forms reactive oxygen species: fats in cell membranes, proteins and genetic material are oxidised, and copper can attach to mitochondrial enzymes and disrupt their work. At the same time glutathione is used up. This is seen most clearly in hereditary Wilson's disease, in which the ATP7B pump in the liver cell does not work and copper is not released into the bile.

The interpretation is given in your report.