Figure 1.

Degradation and resynthesis of ATP via the purine salvage pathway. ATP is degraded to metabolites such as adenosine, inosine or hypoxanthine, which can, via equilibrative transporters, leave cells and enter the blood stream. Purine salvage (blue arrows) restores adenine nucleotide levels via hypoxanthine phosphoribosyltransferase (HPRT; hypoxanthine to IMP) and adenine phosphoribosyltransferase (APRT; adenine to AMP). This reaction (as does de novo purine synthesis) requires 5-phosphoribosyl-1-pyrophosphate (PRPP), a product of the pentose phosphate pathway from which emerges ribose-5-phosphate. An additional source of ribose-5-phosphate is from the isomerisation of inosine-derived ribose-1-phosphate by phosphopentomutase (black dashed line). Adenine, hypoxanthine and D-ribose are precursors, which enter the salvage pathway. Allopurinol inhibits the metabolism of hypoxanthine to xanthine and from xanthine to uric acid. This reduces the production of non-salvageable xanthine, makes more hypoxanthine available for salvage and limits the production of hydrogen peroxide (H₂O₂) and subsequent reactive oxygen species. (1) adenylate kinase, (2) ATPases, (3) 5′nucleotidase, (4) adenosine kinase, (5) adenosine deaminase, (6) purine nucleoside phosphorylase, (7) xanthine oxidase, (8) ribulose 5-phosphate isomerase, (9) ribokinase, (10) phosphoribosylpyrophosphate synthetase, (11) adenylosuccinate synthetase and (12) adenylosuccinate lyase.