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Heme Degradation and Bilirubin Formation
Published in Karel P. M. Heirwegh, Stanley B. Brown, Bilirubin, 1982
A novel feature of the initial reaction of Figure 1 is the elimination of a methene bridge carbon atom of heme as carbon monoxide, leading to the remarkable situation where the highly functional heme is converted to two potentially toxic metabolites. Approximately 0.4 g of bilirubin per day is produced by normal adult humans and this corresponds to about 15 ml of carbon monoxide measured at STP. At any time this carbon monoxide accounts for about 1 to 2 ppm of exhaled gases (a level which is readily measurable). Indeed, hemolytic states may be detected in terms of an increase of exhaled carbon monoxide, although careful corrections for environmental factors such as cigarette smoking must be made. Of course, this level of carbon monoxide is not acutely toxic, since the oxygen concentration in air is about 200,000 ppm and, even allowing for the greater affinity of carbon monoxide, very little hemoglobin is in the carbonmonoxy form. In addition to biliverdin and carbon monoxide, iron is also a product of heme catabolism. Unlike the two former catabolites however, iron is not eliminated from the organism, but is retained in the iron pool presumably being returned to the ferritin stores, probably via transferrin. Indeed the whole of the heme synthetic and degradative pathways can be written as an iron cycle in which iron is conserved.
Ferroportin-inhibitor salt: patent evaluation WO2018192973
Published in Expert Opinion on Therapeutic Patents, 2021
Snehal Kadam, Megha Khaitan, Paromita Banerjee, Anita Mandhare
Recent knowledge about the iron cycle involving binding of the hepcidin hormone with the transmembrane protein, ferroportin expressed on enterocyte, and macrophages to inhibit the function of iron export into the bloodstream, has led to increased interest in therapies directed at the hepcidin–ferroportin axis [12].