Match the metabolic pathway in Figure:17.7 with the reactions listed on 394. Chapter 17 : METABOLISM OF NUCLEOTIDES393AMP deaminaseAMPIMPGMPNH3H20-H2O-NucleotidaseNucleotidasePitNucleotidasePitPitNH2AdenosinedeaminaseHNHNH20NHN'H2NŘiboseŘiboseRiboseAdenosineInosineGuanosinePiN Purine nucleosideRibose +phosphorylaseI-phosphatePiPurinenucleosidephosphorylaseHNRibose1-phosphateНурохanthineH20 + O2XanthineoxidaseHNGuanaseHNNH, HOH2N°N.GuanineXanthineH2O + O2ХanoxidaseH2O,HNN.Uric acidFig. 17.7 : Degradation of purine nucleotides to uric acid (AMP-Adenosine monophosphate;IMP-Inosine monophosphate; GMP-Guanosine monophosphate). 394BIOCHEMISTRYUric acidMost animals (other than primates) however,oxidize uric acid by the enzyme uricase toallantoin, where the purine ring is cleaved.Allantoin is then converted to allantoic acid andUricaseAllantoinexcreted in some fishes (Fig.17.8). Furtherdegradation of allantoic acid may occur toproduce urea (in amphibians, most fishes andsome molluscs) and, later, to ammonia (inmarine invertebrates).AllantoinaseAllantoic acidGlyoxylateAllantoicaseUreaUreaseAmmoniaDISORDERS OFPURINE METABOLISMFig. 17.8 : Degradation of uric acid inanimals other than man.Hyperuricemia and goutUric acid is the end product of purinehumans.1. The nucleotide monophosphates (AMP, metabolismIMP and GMP) are converted to their respective concentration of uric acid in the serum of adultsnucleoside forms (adenosine, inosine andguanosine) by the action of nucleotidase.inThenormalis in the range of 3-7 mg/dl. In women, it isslightly lower (by about 1 mg) than in men. Thedaily excretion of uric acid is about 500-700 mg.2. The amino group, either from AMP oradenosine, can be removed to produce IMP orinosine, respectively.Hyperuricemia refers to an elevation in theserum uric acid concentration. This is sometimesassociated with increased uric acid excretion3. Inosine and guanosine are, respectively, (uricosuria).converted to hypoxanthine and guanine (purinebases) by purine nucleoside phosphorylase. overproduction of uric acid. At the physiologicalAdenosine is not degraded by this enzyme, pH, uric acid is found in a more soluble form asGout is a metabolic disease associated withsodium urate. In severe hyperuricemia, crystalsof sodium urate get deposited in the soft tissues,hence it has to be converted to inosine.4. Guanine undergoes deamination by particularly in the joints. Such deposits areguanase to form xanthine.commonly known as tophi. This causes5. Xanthine oxidase is an important enzyme inflammation in the joints resulting in a painfulthat converts hypoxanthine to xanthine, and gouty arthritis. Sodium urate and/or uric acidxanthine to uric acid. This enzyme contains may also precipitate in kidneys and ureters thatFAD, molybdenum and iron, and is exclusively results in renal damage and stone formation.Historically, gout was found to be oftenassociated with high living, over-eating andtissues. Catalase cleaves H2O2 to H2O and O2. alcohol consumption. In the previous centuries,found in liver and small intestine. Xanthineoxidase liberates H,O2 which is harmful to theUric acid (2,6,8-trioxypurine) is the final alcohol was contaminated with lead during itsexcretory product of purine metabolism inhumans. Uric acid can serve as an importantantioxidant by getting itself converted (non- excretion causing gout. In general, a diet rich isenzymatically) to allantoin. It is believed that theantioxidant role of ascorbic acid in primates isreplaced by uric acid, since these animals havelost the ability to synthesize ascorbic acid.manufacture and storage. Lead poisoning leadsto kidney damage and decreased uric acidmeat and seafoods is associated with increasedrisk of gout.The prevalence of gout is about 3 per 1,000persons, mostly affecting males. Post-menopausal

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DNA and RNA are made up of long chains of nucleotides. Sugar molecule, ribose in RNA, and…