[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Biochemistry](https://durgical.com/en/biochemistry/) › Purine degradation and salvage [Biochemistry](https://durgical.com/en/biochemistry/) · Metabolic pathway # Purine degradation and salvage Spare purines are turned into uric acid, which leaves in the urine; many of the bases are recycled before they get that far. Updated 2026-11-01 ## Interactive map ## Key facts - End product in humans: uric acid. We lack uricase, so blood urate is much higher than in most mammals. - Xanthine oxidase performs the last two steps (hypoxanthine → xanthine → uric acid); allopurinol and febuxostat block it. - Salvage: HGPRT recovers hypoxanthine and guanine (→ IMP, GMP) and APRT recovers adenine (→ AMP), both using PRPP. - Parallel AMP route: AMP → adenosine (5'-nucleotidase) → inosine (adenosine deaminase, ADA). Its deficiency causes severe combined immunodeficiency. - GMP follows: guanosine → guanine (PNP) → xanthine (guanase), joining the same final route. ## In detail - Salvage is cheap: one step with PRPP versus six high-energy bonds for de novo synthesis. - The brain and lymphocytes depend heavily on salvage or de novo synthesis, which is why defects give neurological or immune symptoms. - About two-thirds of urate is excreted by the kidney and the rest through the gut. - In the kidney, the URAT1 transporter reabsorbs urate; it is the target of uricosuric drugs. **Also called** Purine catabolism ## Regulation - The pathway is controlled mainly by supply: more cell turnover or more dietary purine yields more uric acid. - Salvage uses up PRPP; when it fails (HGPRT deficiency), leftover PRPP speeds up de novo synthesis. ## The steps, one by one - **Step 1 · AMP deaminase (AMPD)** irreversible AMP (adenylate) + H₂O → [IMP](https://durgical.com/en/biochemistry/molecules/imp/) + nh3 Removes the amino group of AMP, leaving IMP; very active in muscle during exercise. **If it fails:** Muscle deficiency (AMPD1) is common and usually silent; sometimes it causes cramps with exercise. - **Step 2 · 5'-Nucleotidase** irreversible [IMP](https://durgical.com/en/biochemistry/molecules/imp/) + H₂O → Inosine + phosphate (Pi) Removes the phosphate: the nucleotide becomes a nucleoside (inosine). **If it fails:** Serum 5'-nucleotidase rises in cholestasis. - **Step 3 · Purine nucleoside phosphorylase (PNP)** Inosine + phosphate (Pi) ⇌ [Hypoxanthine](https://durgical.com/en/biochemistry/molecules/hypoxanthine/) + Ribose 1-phosphate Splits the base from the sugar using phosphate, leaving free hypoxanthine. **If it fails:** PNP deficiency builds up dGTP in T cells: cellular immunodeficiency and low uric acid. - **Step 4 · [Xanthine oxidase](https://durgical.com/en/biochemistry/enzymes/xanthine-oxidase/)** irreversible [Hypoxanthine](https://durgical.com/en/biochemistry/molecules/hypoxanthine/) + o2 + H₂O → Xanthine + Hydrogen peroxide First oxidation: hypoxanthine becomes xanthine at the molybdenum centre. **If it fails:** Its deficiency (xanthinuria) lowers uric acid and forms xanthine stones. [Hereditary xanthinuria →](https://durgical.com/en/conditions/hereditary-xanthinuria/) - **Step 5 · [Xanthine oxidase](https://durgical.com/en/biochemistry/enzymes/xanthine-oxidase/)** irreversible Xanthine + o2 + H₂O → [Uric acid](https://durgical.com/en/biochemistry/molecules/uric-acid/) + Hydrogen peroxide Second oxidation by the same enzyme: xanthine becomes uric acid, the human end product. **If it fails:** Excess uric acid precipitates as urate crystals: gout and stones. [Gout →](https://durgical.com/en/conditions/gout/) - **Step 6 · Urate oxidase (uricase): absent in humans** irreversible [Uric acid](https://durgical.com/en/biochemistry/molecules/uric-acid/) + o2 + H₂O → Allantoin + CO₂ + Hydrogen peroxide This step does not exist in humans: it is shown because recombinant uricase (rasburicase) is used as a drug. **If it fails:** Rasburicase is contraindicated in G6PD deficiency: the H₂O₂ it makes causes haemolysis and methaemoglobinaemia. [Tumour lysis syndrome →](https://durgical.com/en/conditions/tumour-lysis-syndrome/) ## Clinical notes - Gout: monosodium urate crystals in joints when urate exceeds its solubility limit. - Tumour lysis syndrome: massive tumour cell death floods the pathway with purines and injures the kidney. - HGPRT deficiency: Lesch-Nyhan syndrome (complete) or juvenile gout (partial). - PNP deficiency: T-cell immunodeficiency with very low uric acid. ## Related conditions - [Gout](https://durgical.com/en/conditions/gout/) - [Kidney stones (urolithiasis)](https://durgical.com/en/conditions/kidney-stones/) - [Lesch-Nyhan syndrome](https://durgical.com/en/conditions/lesch-nyhan-syndrome/) - [Adenosine deaminase deficiency (ADA-SCID)](https://durgical.com/en/conditions/adenosine-deaminase-deficiency/) - [Tumour lysis syndrome](https://durgical.com/en/conditions/tumour-lysis-syndrome/) - [Hereditary xanthinuria](https://durgical.com/en/conditions/hereditary-xanthinuria/) ## Related - [Uric acid](https://durgical.com/en/biochemistry/molecules/uric-acid/) - [Hypoxanthine](https://durgical.com/en/biochemistry/molecules/hypoxanthine/) - [IMP (inosine monophosphate)](https://durgical.com/en/biochemistry/molecules/imp/) - [Xanthine oxidase](https://durgical.com/en/biochemistry/enzymes/xanthine-oxidase/) - [Adenosine deaminase (ADA)](https://durgical.com/en/biochemistry/enzymes/adenosine-deaminase/) - [Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)](https://durgical.com/en/biochemistry/enzymes/hypoxanthine-guanine-phosphoribosyltransferase/) - [Adenine phosphoribosyltransferase (APRT)](https://durgical.com/en/biochemistry/enzymes/adenine-phosphoribosyltransferase/) - [PRPP (phosphoribosyl pyrophosphate)](https://durgical.com/en/biochemistry/molecules/prpp/) - [De novo purine synthesis](https://durgical.com/en/biochemistry/pathways/de-novo-purine-synthesis/) - [Drugs acting on nucleotide metabolism](https://durgical.com/en/biochemistry/topics/drugs-acting-on-nucleotide-metabolism/) ## Test yourself Think of the answer, then tap the question to see it. ## Why does allopurinol lower uric acid? Its metabolite oxypurinol binds tightly to xanthine oxidase and blocks the pathway's last two steps. ## Which enzymes recycle purine bases, and which co-substrate do they use? HGPRT (hypoxanthine, guanine) and APRT (adenine); both use PRPP and form the nucleotide in one step. ## Why do humans have higher urate than most mammals? Uricase was lost in evolution: uric acid is the end product and is not converted to allantoin. [Add to my cards (3)](https://durgical.app/estudiar/?add=/en/biochemistry/pathways/purine-degradation-and-salvage/) Educational information, not medical advice. For any symptom, see a health professional. Sources: [Purine catabolism](https://reactome.org/PathwayBrowser/#/R-HSA-74259) (Reactome, 2026); [Purine salvage](https://reactome.org/PathwayBrowser/#/R-HSA-74217) (Reactome, 2026); [Uric acid - blood: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/003476.htm) (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011). [← All of biochemistry](https://durgical.com/en/biochemistry/) ## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake Representative model, for educational purposes only. --- Source: https://durgical.com/en/biochemistry/pathways/purine-degradation-and-salvage/ License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/biochemistry/pathways/purine-degradation-and-salvage/