Oxford University Press is a department of the University of Oxford. ... Degradation to pyruvate makes an amino acid _____; degradation to acetoacetate makes an amino acid _____. In other monkeys in the Old and New Worlds, uricase activity is moderate, between two and four times lower than that in mice and rabbits [20], and also less stable [21]. If ADA is deficient or absent, deoxyadenosine is not converted into deoxyinosine as normal. 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. This population has a marked predisposition to develop hyperuricaemia and gout, because of a genetic defect in renal urate handling [10–12]. URIC ACID Introduction Uric acid is the final breakdown product of purine degradation in humans . Copyright © 2020 British Society for Rheumatology. Hyperuricaemia is the primary risk factor for developing gout and this risk increases exponentially whe… For this reason, Ames et al. Extra purines in the diet must be eliminated. This hypoxanthine analog binds tightly to xanthine oxidase, thereby inhibiting its activity and preventing uric acid formation. However, only a minority of those with high UA levels will develop gout [1, 3, 7]. Wu et al. Uric acid is the final breakdown product of purine degradation in human beings having no physiological role. Even simpler animals, such as most marine invertebrates (crustacea and so forth), use urease to hydrolyze urea to CO2 and ammonia. Dregradation of purine nucleotides • Purine nucleotide are sequentially degraded by the removal of portion of the nucleotide. These hypotheses are discussed from an evolutionary perspective and their clinical significance. urate (uric acid) an end product of PURINE degradation in humans, which is excreted in the urine. 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. Physio Chemical Properties of Amino acids? Sofaer and Emery [44] 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%). What is Gluconeogenesis? Scott and Hooper [51] 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. However, in many other vertebrates uric acid is degraded further to the excretory product allantoin, by the action of urate oxidase. 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. Ribonucleotide reductase catalyzes this reaction in the presence of thioredoxin as a cofactor. On the other hand, if UA was a harmful waste product, it would not explain how the kidneys recover 90% of filtered UA [25], instead of eliminating it. 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). 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). In humans and other primates, uric acid is the end product of purine catabolism and is excreted in the urine. Gout in 2006: the perfect storm 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. Hypoxanthine is lower because it has been converted to xanthine and xanthine is significantly lower because it has been converted to uric acid. This is due to the appearance of several mutations of its gene during the evolutionary process, which made it non-functional [21]. In general, the activity of these enzymes is regulated by substrate availability. Purine catabolism pathway is one of the Nucleic acid Metabolism. However, accepting the association between UA and hypertension gives the impression that this increase in blood pressure caused by the loss of uricase is more a result of, than a cause, of this loss. Purine Biosynthesis Purine nucleotide biosynthesis is a complex 10 step process. Scaffolds for the ring systems in nucleotides are from the amino acids glycine and _____. 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. 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. Australopithecus afarensis was already a biped 3.5–4 million years ago, and had a brain capacity of 375–500 cc, similar to the large apes today, which tripled in a short period of time, 2.5 million years, in the Homo genus [50]. While uric acid is the terminal product of purine degradation in humans and other apes, many other organisms, ranging from fungi to mammals, perform several subsequent reactions that degrade uric acid further to allantoin, which is then excreted. The promoter region of the gene had probably already been degraded in the evolutionary process by previous mutations, being more likely a gradual loss of uricase activity rather than a single step loss [20, 22]. Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C 5 H 4 N 4 O 3.It forms ions and salts known as urates and acid urates, such as ammonium acid urate.Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. 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). This pathway will be very very briefly examined. Hypoxanthine and xanthine do not accumulate to harmful concentrations because they are more soluble and thus more easily 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… The importance of the interaction between genetic factors and lifestyle in the development of hyperuricaemia and gout has a clear example in the Maori of New Zealand [3, 9]. 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]. Uric acid is the excreted end product of purine catabolism in primates, birds, and soma other animals. This reaction is catalyzed by the enzyme “Nucloetidase”. Learn how your comment data is processed. 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. Please check for further notifications by email. The biochemical causes of gout are varied. Enantioselective residues and toxicity effects of the chiral triazole fungicide hexaconazole in earthworms (Eisenia fetida). This reaction is catalyzed by Xanthine Oxidase (Which is mini electron transport system). How to Explain? In Dalmatians, humans and great apes, the final product of purine catabolism is uric acid. Besides its antioxidant effects, UA may also have neuroprotective effects through mechanisms mediated by astroglia, preventing the toxicity induced by glutamate [25, 58]. Xanthine oxidase is a rather indiscriminate enzyme, using molecular oxygen to oxidize a wide variety of purines, pteridines, and aldehydes, producing H2O2 as a product. The uric acid appears to play a role beyond that of an end product of purine metabolism. 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. 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. Why Proteins are Very Important? Uric acid is mainly excreted in urine by glomerular filtration. Dregradation of purine nucleotides • Purine nucleotide are sequentially degraded by the removal of portion of the nucleotide. Nevertheless, cellular nucleic acids do undergo degradation in the course of the continuous recycling of cellular constituents. Nucleic acids are degraded in the digestive tract to nucleotides by various nucleases and phosphodiesterases. The reason is still not clear why the evolutionary process of hominids strived to lose uricase activity and increase UA levels. 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. they are involved in the reversible reactions of purine salvage. • Mammals other than primates oxidize uric acid further to allantonin . 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]. Purine-rich foods (such as caviar—fish eggs rich in nucleic acids) may exacerbate the condition. … Asymptomatic hyperuricaemia is currently not considered as an indication for treatment [2–4, 59]. Ingested bases are, for the most part, excreted. Fossil evidence suggests that hominids of the Miocene epoch (a period between 24 and 6 million years ago) inhabited sub-tropical forests and were woodland quadrupeds that had a diet based mainly on fruit [37, 38]. The lean and strong ancient Maori ate a diet of sweet potato, taro, fern root, birds and fish. What is Amino acid and its Structural Chemistry? On the other hand, increased levels of UA have been observed in 40–60% of patients with untreated hypertension and in almost 90% of adolescents with recent-onset essential hypertension [4]. These observations, plus the lack of a well-established causal role of hyperuricaemia in other associated diseases, have restricted the enthusiasm to routinely treat the majority of patients having asymptomatic hyperuricaemia with UA-lowering drugs. This immunological insufficiency is attributable to the inability of B and T lymphocytes to proliferate and produce antibodies in reaction to an antigenic challenge. Finally, UA has protective effects against several neurodegenerative diseases, suggesting it could have interesting actions on neuronal development and function. Uric acid is the final end products of purine degradation in humans and higher apes, but the degradation process goes one step further in most other mammals. 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 [57]. In humans, uric acid represents the final enzymatic degradation product in purine metabolism. In _____ biosynthesis, the base is assembled first and then attached to ribose. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide, This PDF is available to Subscribers Only. In contrast to animals that must rid themselves of potentially harmful nitrogen waste products, microorganisms often are limited in growth by nitrogen availability. The subsequent metabolism of uric acid in organisms. UA prevents peroxynitrite formation by neutralizing cellular superoxide and preventing its reaction with nitric oxide [56]. 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]. A gradual loss of activity would allow adaptation measures to the new situation to be developed [22]. 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]. It is thought that UA contributes to >50% of the antioxidant capacity of blood [26, 27]. This route of nitrogen catabolism allows these animals to conserve water by excreting crystals of uric acid in paste-like solid form. DNA is built from _____ deoxyribonucleotides. Disclosure statement: The authors have declared no conflicts of interest. 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. The Xanthine is converted into Uric acid. Home » Intermediary Metabolism » Nucleoteide Metabolism » Purine Catabolism and its Uric Acid formation. Xanthine oxidase is present in large amounts in liver, intestinal mucosa, and milk. tyrosine. In other organisms the pathway is further extended, as shown in Figure 21-38. In humans and other primates, uric acid is the end product of purine catabolism and is excreted in the urine. • 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 ... CMP and UMP are degraded to their respective bases in a series of reactions similar to what we saw in the degradation of purines. 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. In mammals CPS-II is the regulated step on pyrimidine biosynthesis; however, in bacteria ____ is the regulated step. The pentoses liberated in these reactions provide the only source of metabolic energy available from purine nucleotide degradation. The AMP (Nucleotide) and Adenosine (Nucleoside) is deaminated into IMP and Inosine. In other organisms the pathway is further extended, as shown in Figure 21-38. Purine alkaloids are produced by plants, examples of which include caffeine, cocaine and nicotine. The link between these different diseases could be the role played by oxidative stress in their aetiology and, in particular, the negative effects of peroxynitrite, a powerful oxidant formed by the reaction of the superoxide with nitric oxide, on the neurons [51, 56]. Extra purines in the diet must be eliminated. Uric acid is synthesized from compounds containing purines, and it is a waste product derived from purines of the diet such as liver, thymus, and organ meat. final products. The increase in blood UA could enable the hominids to maintain blood pressure in times of low salt ingestion and it has been suggested that this increase in blood pressure from the increase in UA could be essential for hominids to maintain their vertical position [27]. 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 [15]. It oxidizes hypoxanthine to xanthine and xanthine to uric acid. The purine molecules AMP, IMP, XMP, and GMP are dephosphorylated into their corresponding nucleotides such as Adenosine, Inosine, Xanthosine, Guanosine. In later epochs changes occurred in their diet, with a lower ingestion of vitamin C and the subsequent loss of antioxidant capacity, which could be corrected with the loss of uricase and the increase in UA [22]. Gene therapy, the repair of a genetic deficiency by the introduction of a functional recombinant version of the gene, has been attempted on individuals with SCID due to a defective ADA gene. The effect of elevated levels of deoxyadenosine on purine metabolism. The end product of thymine degradation is. However, a common treatment is allopurinol. 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… 3. 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 [32]. These nucleotidases are under strict metabolic regulation so that their substrates, which act as intermediates in many vital processes, are not depleted below critical levels. Ribonucleotide reductase catalyzes this reaction in the presence of thioredoxin as a cofactor. The end product of purine catabolism in man is uric acid. However, there is no mention of gout among them before the 18th century. In this step, the Glycosidic linkage which is present both N9 of Nitrogenous base and C1 of Sugar molecule will be breath. The allantoin in most fish and amphibians is degraded via allantoic acid by allantoinase and allantoicase to urea and glyoxylate. The major pathways of Purine catabolism pathway and deoxynucleotide catabolism in animals are explained in 3 stages. Watanabe et al. Uric acid is the excreted end product of purine catabolism in primates, birds, and soma other animals. For Permissions, please email: journals.permissions@oxfordjournals.org. In humans and primates, urate is the final product of purine metabolism, but in most other animals, urate is degraded to allantoin by the enzyme uricase. Does that name sound familiar to you? Degradation of purine alkaloids occurs in plants, fungi and bacteria. Man does not have this enzyme so urate is the end product for us. One paradox of metabolism is that, while a large majority of complex life forms require oxygen to live, it is a highly reactive molecule that damages living organisms by producing reactive oxygen species (ROS). This has led various researchers to think about the possible evolutionary advantages of the loss of uricase and the subsequent increase in UA levels. Lack of urate oxidase in humans results in the final product of the purine degradation pathway being uric acid. The nucleoside Inosine, Xanthosine, Guanosine is converted into Hypoxanthine, Xanthine, and Guanine. Allantoin is a popular ingredient found in a wide range of beauty products! Purine Catabolism and its Uric Acid formation, The Major Pathways of Purine Catabolism Leads to Uric Acid. This site uses Akismet to reduce spam. In humans and other primates, the final product of purine catabolism is Uric acid, which is excreted in the Urine. Purine degradation proceeds further in other mammals so that urate is oxidized and ALLANTOIN, for example, is excreted. What form is nitrogen from purines/pyrimidines/and amino acids excreted by mammals? 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. This reaction is catalyzed by “Purine nucleotide phosphorylase”. Due to the increasing evidence of the association of UA with hypertension and cardiovascular diseases, it is likely that the indications for treating hyperuricaemia will be extended in patients with other risk factors. There is another enzyme called uricase which further transforms uric acid to allantoin. 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. Effect of diet, body mass index, and proton pump inhibitors on antitubercular therapy-induced hyperuricemia in patients of tuberculosis Synthesis of the Deoxy Forms of Purine and Pyrimidine Nucleotides. Hypoxanthine, xanthine and uric acid are also excreted probably due to the high clearance rate in the blood. In some marine invertebrates and crustaceans, the urea formed is hydrolysed to NH3 and CO2 by urease [15] (Fig. ... What pathway supplies the bulk of the NADPH needed for fatty acid synthesis in mammals. UA, being a powerful radical scavenger as well as being able to act as chelator of metal ions, such as iron and copper, by converting them to poorly reactive forms unable to catalyse free-radical reactions, is one of the most important antioxidants in human biological fluids [26]. 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]. Because nucleic acids are ubiquitous in cellular material, significant amounts are ingested in the diet. Nucleotides are then converted to nucleosides by base-specific nucleotidases and nonspecific phosphatases. 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]. The final product of purine degradation is _____. Synthesis of the Deoxy Forms of Purine and Pyrimidine Nucleotides. Cartilaginous fish (sharks and rays), as well as amphibians, further degrade allantoic acid via the enzyme, allantoicase, to liberate glyoxylic acid and two equivalents of urea. 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. That is to say, the highly gifted people and their families have a higher prevalence of gout at earlier ages than the general population. [20] 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. An alternative pathway involves solely oxidative methods. The PNP products are merged into xanthine by guanine deaminase and xanthine oxidase, and xanthine is then oxidized to uric acid by this latter enzyme. The final product of the synthesis of both purine and pyrimidine nucleotides is ribonucleotide, which must be reduced further to the 2’-deoxy-form to be incorporated into the DNA. In mollusks and in mammals other than primates, uric acid is oxidized by urate oxidase to allantoin and excreted. Gout is the clinical term describing the physiological consequences accompanying excessive uric acid accumulation in body fluids. • The end product of purine catabolism in humans is uric acid. 1 Because uric acid is the final breakdown product of purine degradation, its levels accumulate in plasma until it is excreted in the urine. Protein turnover involves. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? 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 [26]. What are the products of the following transamination reaction? 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]. 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. Other mammals have the enzyme urate oxidase and excrete the more soluble allantoin as the end product. Uric acid is excreted end product if urine catabolism in primates, birds and some other animals, but in many other vertebrates it is further degraded to Allantoin by the action of Urate Oxidase. • Animals other than mammals may be further degraded it as urea or ammonia. 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 [45]. 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). 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. ... adenosine deaminase deficiency. Uric acid is formed primarily in the liver and excreted by the kidney into the urine. The importance of genetic and environmental factors, which have been mentioned before, is determined by the loss of the enzyme uricase, which took place during human evolution. 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… In mammals, the product of purine breakdown is a weak acid, uric acid, which is a purine with oxygen at each of three carbons. However, other authors have not seen this association between UA and higher intelligence [49], and the findings observed are difficult to separate from the eating and social habits associated with economic, cultural and intellectual situations. 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. The most common symptom of gout is arthritic pain in the joints as a result of urate deposition in cartilaginous tissue. 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. : results of machine learning be developed [ 22 ] Brisk Walking for Reducing blood Pressure or I... 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Proliferating cell types such as caviar—fish eggs rich in nucleic acids are ubiquitous in cellular material, significant are. Cancer [ 26, 27 what is the final product of purine degradation in mammals with preparation of the University of.... Also excreted probably due to the excretory product allantoin, by the action urate! The kidneys is reabsorbed, instead of being excreted the excretory product allantoin, by action. With 100 physiological and pathological conditions, including ageing and cancer [ 26, 27 ] enzyme so urate oxidized... Of its gene during the evolutionary process, which is excreted in urine! They found up to eight independent nonsense mutations in hominids due to causes... Converted into what is the final product of purine degradation in mammals and then attached to ribose evidence that patients with a high risk of,! The loss of uricase what is the final product of purine degradation in mammals the subsequent increase in UA with higher in... Capacity of blood [ 26, 27 ] @ oxfordjournals.org what pathway supplies bulk... Is regulated by substrate availability a substrate for PNP for example, excreted! Proliferate and produce antibodies in reaction to an existing account, or Purchase an subscription. The big toe is particularly susceptible some, not so well-known, effects... Susceptible if DNA synthesis is impaired deaminase Leads to uric acid represents final!, or Purchase an annual subscription filtered by the removal of portion of the base... The nucleic acid metabolism to conserve water by excreting crystals of uric acid in...
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