ceruloplasmin
Ceruloplasmin, (Cp) caeruloplasmin, ferroxidase, or iron(II):oxygen oxidoreductase is an acute phase protein synthesized in response to pro-inflammatory cytokines in the inflammatory response (acute and chronic).
Ceruloplasmin (ferroxidase) is an enzyme that catalyzes oxidation of ferrous iron (Fe2+) to ferric iron (Fe3+), rendering iron suitable for binding and plasma transportation by transferrin.
Cp is also reported to oxidize LDL, so, since oxidized LDL (Ox-LDL) is a well-known atherogenic factor, elevated serum Cp is expected to act as an atherogenic factor. Elevated level of Ox-LDL inhibits nitric oxide (NO) production, and a decreased level of NO impairs the endothelium-dependent relaxation of arteries, providing a factor causing atherosclerosis.
Ninety percent or more of total serum copper is located in ceruloplasmin, though albumin is the chief transport protein for copper. Levels of ceruloplasmin are elevated in acute and chronic inflammation, rheumatoid arthritis, lymphoma, carcinomas, leukemia's, Hodgkin disease, primary biliary cirrhosis, systemic lupus erythematosus, pregnancy. Levels are depressed in copper deficiency, Vitamin C overdose, excessive therapeutic zinc, and rare disorders of copper metabolism and/or storage (aceruloplasminemia, Menke's kinky hair syndrome, Wilson's disease (hepatoenticular degeneration)). Aceruloplasminemia is caused by mutations in the gene encoding ceruloplasmin on chromosome 3q (bands 3q23-q25).
tags [Enzymes] [acute phase] [ceruloplasmin] [iron transport] [transferrin] [copper+transport] [inflammation] [cytokine]
Ceruloplasmin (ferroxidase) is an enzyme that catalyzes oxidation of ferrous iron (Fe2+) to ferric iron (Fe3+), rendering iron suitable for binding and plasma transportation by transferrin.
Cp is also reported to oxidize LDL, so, since oxidized LDL (Ox-LDL) is a well-known atherogenic factor, elevated serum Cp is expected to act as an atherogenic factor. Elevated level of Ox-LDL inhibits nitric oxide (NO) production, and a decreased level of NO impairs the endothelium-dependent relaxation of arteries, providing a factor causing atherosclerosis.
Ninety percent or more of total serum copper is located in ceruloplasmin, though albumin is the chief transport protein for copper. Levels of ceruloplasmin are elevated in acute and chronic inflammation, rheumatoid arthritis, lymphoma, carcinomas, leukemia's, Hodgkin disease, primary biliary cirrhosis, systemic lupus erythematosus, pregnancy. Levels are depressed in copper deficiency, Vitamin C overdose, excessive therapeutic zinc, and rare disorders of copper metabolism and/or storage (aceruloplasminemia, Menke's kinky hair syndrome, Wilson's disease (hepatoenticular degeneration)). Aceruloplasminemia is caused by mutations in the gene encoding ceruloplasmin on chromosome 3q (bands 3q23-q25).
tags [Enzymes] [acute phase] [ceruloplasmin] [iron transport] [transferrin] [copper+transport] [inflammation] [cytokine]