Ceruloplasmin is the main copper-containing protein in blood. It plays an important role not only in copper metabolism, but also participates in a number of chemical reactions, which are:

• Limitation of the free iron release (which itself can be toxic)
• Oxidization of vitamin C (ascorbic acid), noradrenaline, serotonin and other biologically active substances
• Deactivation of reactive oxygen species which can “burn” entire cells in the body.

Deficiency of ceruloplasmin is extremely negative: copper ions go out of the blood vessels into the intercellular space (this reduces the copper content in the blood). The body compensates the lack of copper by its increased absorption in the intestine. Copper enters the bloodstream again and because of the lack of ceruloplasmin goes back into the intercellular space. Copper can accumulate in various organs, damaging them.  The effect on the nervous system is particular important.

Such conditions occur because of the lack of copper in the diet or because of congenital genetic dysfunction of the genes responsible for ceruloplasmin formation:

• Nutritional copper deficiency: reduced blood cell count and resistance to anemia treatment!
• Primary genetic ceruloplasmin deficiency manifests as severe lesions of the nervous system, eyelid spasm, visual impairment.
• Wilson-Conovalov disease (defect of the thirteenth chromosome gene) is the disorder in the attachment of copper to ceruloplasmin plus low copper content. As a result, copper is deposited in the liver, kidneys, brain, iris, so functions of all these organs suffer.
• Menkes' disease is the disruption of copper absorption in the intestine, due to which the production of ceruloplasmin decreases and the physiological functions of this protein cannot be properly performed. It is clinically manifested by mental and physical developmental delays.