Carbon monoxide and bilirubin production in neonates.
Neonatal hyperbilirubinemia is a normal postnatal phenomenon resulting from a transitional imbalance between the production and elimination of bilirubin in the neonate. Bilirubin has been shown to be not only a potent antioxidant, but also toxic at excessive concentrations. As a result, the biology of bilirubin, its production, regulation, and measurements have been the focus of extensive studies. Bilirubin, carbon monoxide, and iron are derived from the degradation of heme, a ubiquitous two-step pathway catalyzed by the enzyme, heme oxygenase. It has been shown that these metabolically active products from the heme catabolic pathway may, in turn, influence many other biologic processes. This report provides a brief overview of these interrelationships in the hope that it may provide insight into the central role this pathway plays in the existence of most organisms.
Stevenson
D K
DK
Department of Pediatrics, Stanford University School of Medicine, CA 94304-1510, USA. dstevenson@stanford.edu
Vreman
H J
HJ
Wong
R J
RJ
Contag
C H
CH
D000818:Animals; D001663:Bilirubin / Q000096:biosynthesis* / Q000097:blood; D002248:Carbon Monoxide / Q000378:metabolism*; D006418:Heme / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D007501:Iron / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism
D007527:Isoenzymes; D006418:Heme; D002248:Carbon Monoxide; D007501:Iron; D006419:Heme Oxygenase (Decyclizing); D001663:Bilirubin