Cerulopshasmine is a ferment with a high copper content, manifesting an increased ferroxidase activity, which is detected as a soluble isoform in plasma or as a membrane-associated isoform in different cell types. The ceruloplasmin-ferroportin system is the main route of cellular iron exit in vertebrates and is responsible for the physiological regulation of cellular iron levels. Ceruloplasmin is a copper-containing ferroxydase and plays an important role in the ionic state regulation of iron oxidation - Fe2+ to Fe3+. As a result, iron is incorporated into transferrin without the formation of toxic iron products. Maintaining the normal transport and metabolism of iron is a function of ceruloplasmin to maintain the vitality of tissues and organs. This review focuses on the structural and functional characteristics of the two proteins, with special emphasis on their coordinated regulation at the transcriptional and post-transcriptional level. Ceruloplasmin (CP) is a glycoprotein that plays an essential role in iron homeostasis. According to the accepted theory, the bivalent iron transported from the cell by ferritin, it is necessary to oxidize certainly by ceruloplasmin in order to slightly facilitate the activity of transferrin. Therefore, the ceruloplasminferoportin system is the main pathway of cellular iron metabolism and is responsible for regulating iron levels in the cell. Oxygen is a paradox for cells in that it is both an essential nutrient needed for survival and a precursor for toxic, potentially deadly byproducts. Ceruloplasmin represents a protein with specific domains capable of both facilitating the production of cellular energy and preventing the formation of oxygen radicals. This ability to perform dual tasks lies in the complex shape and structure of the protein and involves strategically placed copper ions, which can help both give and take up electrons from substrates, including iron, oxygen, and iron-binding proteins. Copper is the essential element for the wide range of ceruloplasmin activities that maximizes iron metabolism. A defect or mutation in the ceruloplasmin gene that denies copper incorporation into ceruloplasmin disrupts iron metabolism. Ceruloplasmin is also involved in many redox reactions. Its effect as a pro-oxidant or antioxidant is due to the presence of other factors. In the presence of superoxide (for example, in the inflamed vascular endothelium), it will act as an oxidation catalyst for low-density lipoproteins. About 95% of all copper in the body is found in connection with apoceruloplasmin, therefore, determining the amount of ceruloplasmin is one of the main methods of assessing copper exchange.