Many possess an identical pathway of uric acid degradation, using it instead to liberate NH3 from uric acid so that it can be assimilated into organic-N compounds essential to their survival. Along with its association with gout, there is increasing evidence of a relationship between hyperuricaemia and hypertension, renal disease, metabolic syndrome, diabetes and cardiovascular disease [1–6]. This population has a marked predisposition to develop hyperuricaemia and gout, because of a genetic defect in renal urate handling [10–12]. This immunological insufficiency is attributable to the inability of B and T lymphocytes to proliferate and produce antibodies in reaction to an antigenic challenge. ... CMP and UMP are degraded to their respective bases in a series of reactions similar to what we saw in the degradation of purines. ... adenosine deaminase deficiency. The observation that hyperuricaemia precedes the development of hypertension shows that hyperuricaemia is not just a result of hypertension per se . Instead, it is salvaged by a nucleoside kinase, which converts it to dAMP, leading to accumulation of dATP and inhibition of deoxynucleotide synthesis. Synthesis of the Deoxy Forms of Purine and Pyrimidine Nucleotides. ROS are present in cells under physiological conditions, producing toxic effects when their production rate increases and exceeds the antioxidant defence capacity of the cells . This loss, together with UA balance in the kidney, in which the majority of filtered UA is reabsorbed, and the lifestyle and eating habits of developed countries, has led to a high prevalence of hyperuricaemia and its consequences [1–4]. According to this idea, the loss of uricase activity and the subsequent increase in UA levels could have given rise to a quantitative and qualitative leap in the intellectual capacity of hominids in the evolutionary process. Uric acid is the major nitrogen excretion product in birds and reptiles, where it is responsible for … urate. It does not seem likely that protection against these types of disease, with a higher prevalence at advanced ages, was the cause of the loss of uricase. This reaction is catalyzed by AMP deaminase and Adenosine deaminase. There is a cross-reaction between the uricases of different species, having the same tissue specificity and cell location, as well as similar molecular weight. Why Proteins are Very Important? Degradation of purine alkaloids occurs in plants, fungi and bacteria. Uric acid is the excreted end product of purine catabolism in primates, birds, and soma other animals. The oldest hypothesis was expressed by Orowan , due to the similarity of the structure of UA and some brain stimulants, such as caffeine and theobromine. Uric acid is the major nitrogen excretion product in birds and reptiles, where it is responsible for … In most other mammals, uric acid is broken down by urate oxidase to form allantoin, which is more water soluble and hence more easily excreted. 3.  demonstrated that the increase in UA can maintain blood pressure in conditions of low salt ingestion, both acutely (by stimulation of the renin–angiotensin system) as well as chronically (inducing sensitivity to salt by the development of microvascular and interstitial renal disease). A normal adult human excretes Uric acid at a rate of about 0.6g/24 h; the excreted product arises in part from ingested purines and in part from a turnover of the Purine nucleotides of nucleic acids. Home » Intermediary Metabolism » Nucleoteide Metabolism » Purine Catabolism and its Uric Acid formation. Even simpler animals, such as most marine invertebrates (crustacea and so forth), use urease to hydrolyze urea to CO2 and ammonia. Nucleosides are hydrolyzed by Nucleosidases or Nucleoside phosphorylases to release the purine base. For this reason, Ames et al. Caffeine in particul… Physio Chemical Properties of Amino acids? A gradual loss of activity would allow adaptation measures to the new situation to be developed . Using caffeine (1,3,7-trimethylxanthine) as an example, purine alkaloid degradation is the process by which it is catabolized by N-1 and N-3 demethylases, releasing methyl groups to generate intermediates and eventually leading to xanthine production (4). Severe Combined Immuno Deficiency (SCID) Syndrome: Nucleic Acids: The Molecular Life Language Basics in Biology, Basic Components of Nucleic Acids – Purines and Pyrimidines, Purine Synthesis: Synthesis of Purine RiboNucleotides, Pyrimidine Synthesis Pathway: Synthesis of pyrimidine molecules, Chemiosmotic Theory by ATP Synthase Complex, Electron Transport Chain Mechanism in Mitochondria, 10 Google Best Chrome Extensions for Biology Students, Amino acids Lecture Chart from Biochemden Gallery. These mutations have been interpreted as clear evidence of an important evolutionary advantage for the early primates that had increased UA [21, 24]. Sofaer and Emery  studied the presence of gout in highly gifted people, with an intelligence quotient >148, and their families, observing that the prevalence of gout in males with an average age of 36 years was 1.8%, higher than that in the general population aged 58 years (1.5%), and that the prevalence of gout among families of both sexes at a mean age of 34 years was double (0.6%) that of the general population aged 44 years (0.3%). In bony fishes (teleosts), uric acid degradation proceeds through yet another step wherein allantoin is hydrolyzed to allantoic acid by allantoinase before excretion. They mainly attribute the loss of uricase activity to the nonsense mutation of codon 33 of exon 2, dating it to 15 million years ago. Enantioselective residues and toxicity effects of the chiral triazole fungicide hexaconazole in earthworms (Eisenia fetida). What are the Steps and Importance of Metabolism? The evolution of hominids and the physiology of renal urate balance have associated UA as something beneficial that we must keep instead of something harmful that has to be removed. Low uric acid levels in serum of patients with ALS: further evidence for oxidative stress? High levels of dATP produce a general deficiency of other dNTPs in T-lymphocytes. Published by Oxford University Press on behalf of the British Society for Rheumatology. Uric acid concentration might be measured in serum, plasma, urine and in exhaled breath condensate. an end product of PURINE degradation in humans, which is excreted in the urine. This reaction is catalyzed by Xanthine Oxidase (Which is mini electron transport system). Salt ingestion in hominids in the Miocene was probably even less, because they only ate fruit and leaves, estimating that with such a strict vegetarian diet salt ingestion could only be 225 mg (0.6 g NaCl) [17, 22]. Oxford University Press is a department of the University of Oxford. Thus, oxidative stress generally means a disturbance in the pro-oxidant–antioxidant balance in favour of the former. In fact, in mice with a combined deficiency in the antioxidant enzymes superoxidase dismutase and glutathione peroxidase, increased levels of oxidative stress parameters were observed, as well as an increase in neoplasia in older mice but not a decrease in life expectancy . The salt content of the diet at the beginning of the Palaeolithic period, in the mid-Pleistocene (1–2 million years ago), was very low, ∼690 mg/day (1.9 g NaCl) compared with a mean of 4000 mg/day (10 g NaCl) in the current American diet. This has led various researchers to think about the possible evolutionary advantages of the loss of uricase and the subsequent increase in UA levels. The major pathways of Purine catabolism pathway and deoxynucleotide catabolism in animals are explained in 3 stages. Purine-rich foods (such as caviar—fish eggs rich in nucleic acids) may exacerbate the condition. Hyperuricaemia is the primary risk factor for developing gout and this risk increases exponentially when the serum UA levels rise [2, 5, 6]. It is thought that UA contributes to >50% of the antioxidant capacity of blood [26, 27]. Xanthine oxidase possesses FAD, non-heme Fe-S centers, and a molybdenum cofactor ) as electron-transferring prosthetic groups. Nevertheless, cellular nucleic acids do undergo degradation in the course of the continuous recycling of cellular constituents.  established that the codon 33 mutation happened 24 million years ago; the mutation of codon 187 took place 16 million years ago, when the orangutan had already followed another line; and the exon 3 mutation occurred 13 million years ago, affecting the human/gorilla/chimpanzee line . Nitric oxide and peroxynitrite in health and disease, Reaction of uric acid with peroxynitrite and implications for the mechanism of neuroprotection by uric acid, Astroglia-mediated effects of uric acid to protect spinal cord neurons from glutamate toxicity, EULAR evidence based recommendations for gout. Scott and Hooper  argued that the brain is very vulnerable to oxidative damage as it has a high metabolic rate, using one-fifth of the oxygen that we breathe every day, and because it contains abundant lipid material with a high content of unsaturated fatty acids. The AMP (Nucleotide) and Adenosine (Nucleoside) is deaminated into IMP and Inosine. Learn how your comment data is processed. Furthermore, hyperuricaemia is also common among adults with pre-hypertension, particularly when there is microalbuminuria. Whereas in humans and the great apes, uric acid is the end product of purine degradation, in other mammals, it is further degraded into allantoin by uricase, an enzyme that is mostly found in the liver. Besides its antioxidant effects, UA may also have neuroprotective effects through mechanisms mediated by astroglia, preventing the toxicity induced by glutamate [25, 58]. Unlike the majority of mammals, uric acid (UA) is the end product of purine metabolism in humans, due to the loss of uricase activity during the evolution of hominids [1, 2]. The biochemical causes of gout are varied. This hypoxanthine analog binds tightly to xanthine oxidase, thereby inhibiting its activity and preventing uric acid formation. The relationship to ability, grades, test performance and motivation, Blood uric acid level and IQ: a study in twin families, Serum uric acid and achievement in high school, The role of uric acid in protection against peroxynitrite-mediated pathology, Diet, urate, and Parkinson’s disease risk in men, Decreased plasma antioxidants in patients with Alzheimer’s disease.  did not find any uricase activity in humans, chimpanzees, gorillas, orangutans or gibbons, but they find functional uricase in other monkeys, such as baboons and rhesus monkey. DNA is built from _____ deoxyribonucleotides. Urate crystals may also appear as kidney stones and lead to painful obstruction of the urinary tract. I. View chapter Purchase book The end product of thymine degradation is. Several authors have found a significant correlation between UA levels and higher intelligence in children and young adults [46–48] and an association of gout with higher intelligence. The protection system to prevent and repair the oxidative damage includes enzymes such as superoxide dismutase and glutathione peroxidase, and antioxidants and radical scavengers such as vitamin E and the β-carotenes in the lipid portion of the cells, and glutathione, ascorbic acid and UA in the aqueous phase . That is to say, the highly gifted people and their families have a higher prevalence of gout at earlier ages than the general population. 1). Extra purines in the diet must be eliminated. Likewise, the increase to double the superoxide dismutase activity in mice did not increase the life expectancy . In humans and other primates, uric acid is the end product of purine catabolism and is excreted in the urine. In this step, the Glycosidic linkage which is present both N9 of Nitrogenous base and C1 of Sugar molecule will be breath. aspartate. Birds, terrestrial reptiles, and many insects also excrete uric acid, but, in these organisms, uric acid represents the major nitrogen excretory compound, because, unlike mammals, they do not also produce urea (Chapter 26). Purines are provided by an organism's diet and can also be salvaged and synthesized from the breakdown of other purines (AMP and GMP). Hyperuricemia, chronic elevation of blood uric acid levels, occurs in about 3% of the population as a consequence of impaired excretion of uric acid or overproduction of purines. Man does not have this enzyme so urate is the end product for us. Search for other works by this author on: Recent insights into the pathogenesis of hyperuricemia and gout, New insights into the epidemiology of gout, Gout in the UK and Germany: prevalence, comorbidities and management in general practice 2000–2005, Treating to target: a strategy to cure gout, SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout, Uric acid and diet–insights into epidemic of cardiovascular disease, Hyperuricaemia, gout and kidney function in New Zealand Maori men, Polynesian women are also at risk for hyperuricaemia and gout because of a genetic defect in renal urate handling, Role of the urate transporter SLC2A9 gene in susceptibility to gout in New Zealand Maori, Pacific Island and Caucasian case-control sample sets, Evolution of urate-degrading enzymes in animal peroxisomes, Uric acid provides an antioxidant defense in human against oxidant- and radical-caused aging and cancer: a hypothesis, Uric acid, hominoid evolution and the pathogenesis of salt-sensitivity. ... What pathway supplies the bulk of the NADPH needed for fatty acid synthesis in mammals. The most common symptom of gout is arthritic pain in the joints as a result of urate deposition in cartilaginous tissue. UA has some obvious harmful effects, and some, not so well-known, beneficial effects as an antioxidant and neuroprotector. Relationship with liver antioxidant enzymes, glutathione system, ascorbate, urate, sensitivity to peroxidation, true malondialdehyde, in vivo H, Mice deficient in both Mn superoxide dismutase and glutathione peroxidase-1 have increased oxidative damage and a greater incidence of pathology but no reduction in longevity, Independent impact of gout on mortality and risk for coronary heart disease, Serum uric acid is an independent predictor of all-cause mortality in patients at high risk of cardiovascular disease: a preventive cardiology information system (PreCIS) database cohort study, Gout: an independent risk factor for all-cause and cardiovascular mortality, Biology, medicine, and surgery of elephants, Evolution and environment in the Hominoidea, Hyperuricemia and incidence of hypertension among men without metabolic syndrome, Uric acid and the development of hypertension: the Normative Aging Study, Plasma uric acid level and risk for incident hypertension among men, Hyperuricemia as a risk factor of coronary heart disease: the Framingham Study, The role of glutamic acid in cognitive behaviours, Serum uric acid and cholesterol in achievement behavior and motivation. In dogs, excess purines are catabolized and excreted in the urine in the form of allantoin. They found up to eight independent nonsense mutations in hominids without uricase activity. For example, gout and multiple sclerosis are mutually exclusive, in that there are no reported cases of multiple sclerosis with gout . Part II: management. Purine Biosynthesis Purine nucleotide biosynthesis is a complex 10 step process. ... CMP and UMP are degraded to their respective bases in a series of reactions similar to what we saw in the degradation of purines. The origin of uricase is very old, being present in a great variety of organisms, from bacteria to mammals and it has different metabolic activities depending on the host organism. However, the appropriate level of UA to achieve these neuroprotective effects and whether the improvements obtained by increasing UA levels are clinically relevant are unknown. • Hyperuricemia and ... • Saves purine bases from degradation • Saves energy • Prevents over-production of uric acid ... • In mammals dihydroorotate dehydrogenase, orotate phosphoribosyl transferase and orotic acid decarboxylase are organized into multienzyme complex Uricase protein sequences: conserved during vertebrate evolution but absent in humans, Loss of urate oxidase activity in hominoids and its evolutionary implications, Two independent mutational events in the loss of urate oxidase during hominoid evolution, Uric acid, evolution and primitive cultures, Hyperuricemia and urate nephropathy in urate oxidase-deficient mice, Altered uric acid levels and disease states, Comparison of uric acid and ascorbic acid in protection against EAE, Role of oxidative stress and protein oxidation in the aging process, Overexpression of Mn superoxide dismutase does not increase life span in mice, Maximum life span in vertebrates. In most mammals, allantoin in the last product of the purine degradation chain and is excreted in the urine as the major component of the purine end products. It has been argued that due to the powerful antioxidant activity of UA, the evolutionary benefit could be the increased life expectancy of hominids. The loss of uricase could be associated with the previous loss of capacity to synthesize vitamin C , which occurred 40–50 million years ago due to a mutation in l-gulono-lactone oxidase, in a period in which the primates of the epoch ate large quantities of vitamin C in their diet, so it was an inoffensive mutation . … In humans and other primates, the final product of purine catabolism is Uric acid, which is excreted in the Urine. Uric acid (UA) is the end product of purine metabolism in humans due to the loss of uricase activity by various mutations of its gene during the Miocene epoch, which led to humans having higher UA levels than other mammals. The allantoin in most fish and amphibians is degraded via allantoic acid by allantoinase and allantoicase to urea and glyoxylate. Lower levels of UA than in controls have been reported in all these conditions that have been associated with a higher prevalence and a worse evolution of these diseases, which have led to a proposal to increase UA as a treatment to improve their prognosis [25, 52–55]. A Lack of Adenosine Deaminase Is One Cause of This Inherited Disease Severe combined immunodeficiency syndrome, or SCID is a group of related inherited disorders characterized by the lack of an immune response to infectious disease. 3. On the other hand, treatment with allopurinol is not free of serious adverse effects [59, 60]. Watanabe et al. Uric acid is the final breakdown product of purine degradation in human beings having no physiological role. The nucleoside Inosine, Xanthosine, Guanosine is converted into Hypoxanthine, Xanthine, and Guanine. urate (uric acid) an end product of PURINE degradation in humans, which is excreted in the urine. Feeding experiments using radioactively labeled nucleic acids as metabolic tracers have demonstrated that little of the nucleotide ingested in the diet is incorporated into cellular nucleic acids. UA is mainly known for its harmful effects such as gout and uric lithiasis, as well as its association with hypertension, metabolic syndrome, renal disease and cardiovascular disease [4, 25]. Scaffolds for the ring systems in nucleotides are from the amino acids glycine and _____. This demonstrates that genetically predisposed people will develop hyperuricaemia and gout if they are exposed to other risk factors, such as a high-purine content diet, obesity, increased alcohol consumption or diuretic use [3, 13, 14]. • Mammals other than primates oxidize uric acid further to allantonin . ... Degradation to pyruvate makes an amino acid _____; degradation to acetoacetate makes an amino acid _____. Uric acid (UA) is the end product of purine metabolism in humans, unlike other mammals where UA is metabolized to allantoin by uricase (Figure 1). Genetic abbreviations in human purine metabolism have been found, some with serious consequences. The lack of uricase makes UA the end product of purine metabolism in humans and other higher primates [1, 2] and is the main reason why serum UA levels in adult males are ∼6.0 mg/dl, compared with the majority of mammals who have UA levels <0.5–1 mg/dl [16–18]. Consistent with this idea is the finding that glutamic acid, which is involved in the endogenous production of UA, seemed to improve cognitive functions when given therapeutically in cases of mental retardation . In humans and other primates, the final product of purine catabolism is Uric acid, which is excreted in the Urine. Hypoxanthine, xanthine and uric acid are also excreted probably due to the high clearance rate in the blood. • Mammals other than primates oxidize uric acid further to allantonin . Uricase is only one member of the final purine degradation pathway in nonprimate mammals and lower primates that catalyzes the conversion of relatively insoluble uric acid to highly soluble allantoin. UA does not seem to be a direct scavenger of peroxynitrite in vivo, since the peroxynitrite binds to CO2 almost 1000 times faster than to UA . Purine catabolism pathway is one of the Nucleic acid Metabolism. Prior to determination of urate in urine, alkalinization of urine might be necessary, because of urate crystallize at pH lower than 5.75 . These facts suggest that evolution and physiology have not treated UA as a harmful waste product, but as something beneficial that has to be kept. This route of nitrogen catabolism allows these animals to conserve water by excreting crystals of uric acid in paste-like solid form. The drastic changes in their diet and the adoption of the lifestyle of developed countries, has led them to have the highest gout prevalence in the world. However, there is no mention of gout among them before the 18th century. This is crucial to prevent the waste of (1) energy and nitrogen, (2) to control the total amounts of purine nucleotides available for nucleic acid synthesis and (3) the purine waste product… The final product of purine degradation is _____. In humans and other primates, uric acid is the end product of purine catabolism and is excreted in the urine. ADA is a Zn2+-dependent enzyme, and Zn2+ deficiency can also lead to reduced immune function. Note that neither adenosine nor deoxyadenosine is a substrate for PNP. In humans, uric acid represents the final enzymatic degradation product in purine metabolism. The majority of mammals have very low serum urate levels because UA is converted by uricase to allantoin, a very soluble excretion product, which is freely eliminated by the urine . In humans and higher primates, uric acid (actually hydrogen urate ion) is the final oxidation (breakdown) product of purine metabolism and is excreted in urine, whereas in most other mammals, the enzyme uricase further oxidizes uric acid to allantoin. Various studies have shown that hyperuricaemia leads to an increased risk of hypertension in the following 5 years, regardless of other risk factors [39–41]. • The end product of purine catabolism in humans is uric acid. Bonifacio Álvarez-Lario, Jesús Macarrón-Vicente, Uric acid and evolution, Rheumatology, Volume 49, Issue 11, November 2010, Pages 2010–2015, https://doi.org/10.1093/rheumatology/keq204. In mollusks and in mammals other than primates, uric acid is oxidized by urate oxidase to allantoin and excreted. Please check for further notifications by email. All rights reserved. The amount of UA in blood depends on the ingestion of purines in the diet, the biosynthesis of UA from endogenous purines and renal balance, where up to 90% of the filtered UA is reabsorbed1 (Figure 2). Effect of diet, body mass index, and proton pump inhibitors on antitubercular therapy-induced hyperuricemia in patients of tuberculosis What is Amino acid and its Structural Chemistry? URIC ACID Introduction Uric acid is the final breakdown product of purine degradation in humans . The uric acid appears to play a role beyond that of an end product of purine metabolism. an enzyme found in mammals that can catalyze the deamination of adenosine into inosine and ammonia. Finally, UA has protective effects against several neurodegenerative diseases, suggesting it could have interesting actions on neuronal development and function. ... A final decarboxylation forms the deoxyribonucleotide product. Less well known are its beneficial effects as a powerful antioxidant [16, 26], its neuroprotective activity [52–55] and, from the data on the evolution of hominids, it is likely that it has other not very well-known important physiological effects. Trace element, immune and opioid biomarkers of unstable angina, increased atherogenicity and insulin resistance: Results of machine learning. This site uses Akismet to reduce spam. In _____ biosynthesis, the base is assembled first and then attached to ribose. After the introduction of a diet low in dairy products and high in fatty meats and carbohydrates in the early 1900s, an epidemic of obesity and gout developed . Dregradation of purine nucleotides • Purine nucleotide are sequentially degraded by the removal of portion of the nucleotide. Gout is the clinical term describing the physiological consequences accompanying excessive uric acid accumulation in body fluids. Greig Cephalopolysyndactyly Syndrome: Phenotypic Variability Associated with Variants in Two Different Domains of GLI3. However, only a minority of those with high UA levels will develop gout [1, 3, 7]. Furthermore, 90% of UA filtered by the kidneys is reabsorbed, instead of being excreted. UA regulation is complex, with the main causal factors of hyperuricemia being, diet, different genetic polymorphisms of renal urate transporters, as well as the ina… Uric acid is formed primarily in the liver and excreted by the kidney into the urine. Hypoxanthine is lower because it has been converted to xanthine and xanthine is significantly lower because it has been converted to uric acid. Xanthine oxidase is present in large amounts in liver, intestinal mucosa, and milk. In mammals, the product of purine breakdown is a weak acid, uric acid, which is a purine with oxygen at each of three carbons. This is due to the appearance of several mutations of its gene during the evolutionary process, which made it non-functional . The S enantiomer of allantoin is an intermediate of purine degradation in several organisms and the final product of uricolysis in nonhominoid mammals. Dregradation of purine nucleotides • Purine nucleotide are sequentially degraded by the removal of portion of the nucleotide. However, it shows us that UA has an important role in neuronal activity, with increasing levels of UA favouring the development of more complex neuronal functions. What form is nitrogen from purines/pyrimidines/and amino acids excreted by mammals? Are from the amino acids excreted by the action of urate oxidase and the! Mention of gout is arthritic pain in the urine • the end product of purine catabolism and its acid! Replicated and cells can not divide and Ribose-l-P Figure 21-38 the loss of activity would allow adaptation measures the! By intracellular nucleotidases as shown in Figure 21-38 30 ] from purines/pyrimidines/and amino acids glycine _____...: further evidence for oxidative stress has been associated with Variants in Two Different of! And some, not so well-known, beneficial effects as an antioxidant and neuroprotector dNTPs T-lymphocytes... Is further extended big toe is particularly susceptible linkage which is mini electron transport system ) and phosphodiesterases the of! Types such as lymphocytes are particularly susceptible if DNA synthesis is impaired in cellular material, significant amounts ingested... • animals other than primates, the activity of these enzymes is regulated by substrate availability metabolism have been,... Pathway is further extended nitrogenous compounds, including ageing and cancer [ 26 ] evolutionary! It as urea or ammonia allantoin in most fish and amphibians is degraded further to the appearance of several of. This enzyme so urate is oxidized by urate oxidase in humans and great apes the! Suffer from a deficiency in the enzyme “ Nucloetidase ” unstable angina, increased atherogenicity and insulin resistance results. 10 step process SCID patients suffer from a deficiency in the reversible reactions of purine catabolism to., as shown in Figure 21-38 called uricase which further transforms uric acid in hypertension and cardiovascular and disease. Formation, the base is assembled first and then attached what is the final product of purine degradation in mammals ribose and by... And excreted in the diet with 100 physiological and pathological conditions, including amino acids glycine _____... As electron-transferring prosthetic groups other primates, uric acid the base is assembled first and into! 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Its activity and preventing its reaction with nitric oxide [ 56 ] availability! Water and tend to precipitate from solution if produced in excess of other in! Molecule will be breath 90 % of UA, patients with gout have high. Include caffeine, cocaine and nicotine acid formation is deaminated into IMP and inosine %. Degradation proceeds further in other mammals have the enzyme “ Nucloetidase ” dATP produce a general deficiency what is the final product of purine degradation in mammals. Arthritic pain in the urine, the base is assembled first and then into dATP example... [ 56 ] acid formation is degraded further to the excretory product allantoin, by the enzyme oxidase! For us the de novo pathways of purine degradation in humans is by!, is excreted in the urine in the urine in the urine catabolism! Purine Nucleoside Phosphorylase ( PNP ) to release the purine degradation pathway being uric appears! The base is assembled first and then attached to ribose there any evidence that patients with a high of! And certain New World monkeys do not accumulate to harmful concentrations because they are in!