Adenine nucleotide catabolism in human erythrocytes: pathways and regulation.
Studies are reviewed which show that in human erythrocytes the catabolism of AMP, leading to hypoxanthine, proceeds by way of AMP deaminase under physiological conditions as well as upon alkalinization and addition of deoxyadenosine. In contrast, the catabolism induced by glucose deprivation, proceeds for 75% via dephosphorylation of AMP. These findings can be explained by the kinetic properties of erythrocytic AMP deaminase, which were investigated at concentrations of substrate and effectors in the physiological range.
van den Berghe
G
G
Laboratory of Physiological Chemistry, International Institute of Cellular and Molecular Pathology, Brussels, Belgium.
Bontemps
F
F
D000227:Adenine Nucleotides / Q000378:metabolism*; D000241:Adenosine / Q000378:metabolism; D058892:Adenosine Deaminase Inhibitors; D000248:Adenosine Kinase / Q000037:antagonists & inhibitors; D000249:Adenosine Monophosphate / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D006868:Hydrolysis; D007042:Hypoxanthines / Q000378:metabolism; D007700:Kinetics; D009708:Nucleotidases / Q000378:metabolism; D015649:Pentostatin / Q000494:pharmacology; D010766:Phosphorylation; D014372:Tubercidin / Q000494:pharmacology
D000227:Adenine Nucleotides; D058892:Adenosine Deaminase Inhibitors; D007042:Hypoxanthines; D015649:Pentostatin; D000249:Adenosine Monophosphate; D000248:Adenosine Kinase; D009708:Nucleotidases; D000241:Adenosine; D014372:Tubercidin