The following pathways account for the degradation of endogenous purine nucleotides, as well as of the free bases that result from the phosphorolysis of dietary ones. The AMP deaminase reaction is shown in the next slide; the adenosine deaminase reaction is analogous. Partial proteolysis, or the introduction of a strategic disulfide bond, prevent the interaction of the enzyme with NAD+, and the molecule then switches to O2 reduction, as shown in this slide. Nucleosides and free bases that arise during the degradation of nucleic acids and nucleotides can be salvaged and reused. The latter enzyme also occurs in a second variation, which arises through protein modification.


The oxidase activity is found in extracellular enzyme molecules, which lack a supply of NAD+ anyway. Xanthine dehydrogenase or oxidase both can convert hypoxanthine to xanthine and the latter to uric acid.
Typically, when present in the lumen of the tubule, such compounds will compete with urate for reuptake; this is the mode of action of uricosuric drugs like benzbromarone or probenecid. The reason for their delayed discovery is that urate oxidase alone is sufficient for the conversion of urate to allantoin, since the subsequent reactions also occur spontaneously.
This scheme shows the reactions involved in purine salvage, which produce AMP, GMP and IMP.


Intracellularly, most enzyme molecules function as a dehydrogenase and reduce NAD+, as shown in the previous slide.
The major difference is that the spontaneous decay produces allantoin as a racemic mixture, whereas enzymatic formation gives rise to one enantiomer only.



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