Xanthine oxidoreductase (XOR / XDH-XO)
Cofactors used
Clinical / pharmacological. Target of allopurinol and febuxostat; deficiency causes xanthinuria
What it does, reaction by reaction
Purine Degradation (to Uric Acid) Nucleotide Metabolism · Cytosol
Hypoxanthine → xanthine
Converts Hypoxanthine into Xanthine
› Notes
Xanthine oxidoreductase (XOR) catalyzes hypoxanthine + H2O + oxidized electron acceptor → xanthine + reduced electron acceptor. As xanthine dehydrogenase, XOR can transfer electrons to NAD+; as xanthine oxidase, it transfers electrons to O2, generating superoxide and/or H2O2. The molybdenum cofactor, FAD, and iron-sulfur centers are required.
Xanthine → uric acid (urate)
Converts Xanthine into Uric acid
› Notes
XOR catalyzes xanthine + H2O + oxidized electron acceptor → uric acid + reduced electron acceptor. This is the terminal oxidation in humans and is effectively irreversible; uric acid is largely deprotonated to monosodium urate in extracellular fluid.
Showing all 2 reactions.
What accelerates and inhibits it
Regulation is pathway-specific, so each context is listed separately
Purine Degradation (to Uric Acid)
Listed there as: Xanthine oxidoreductase
Hypoxanthine/xanthine availability; conversion of dehydrogenase to oxidase can occur with oxidation/proteolysis
Allopurinol (via oxypurinol), febuxostat, topiroxostat
No dominant acute hormonal regulation; expression can rise with inflammatory and hypoxic/ischemic stress.
Recent literature
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