Asymptomatic hyperuricaemia is currently not considered as an indication for treatment [2–4, 59]. Guanine (nitrogenous base only) is deaminated into Xanthosine in the presence of the “Guanosine deaminase”. Furthermore, 90% of UA filtered by the kidneys is reabsorbed, instead of being excreted. Purine degradation proceeds further in other mammals so that urate is oxidized and ALLANTOIN, for example, is excreted. Uric acid is the major nitrogen excretion product in birds and reptiles, where it is responsible for … 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]. 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]. Protein turnover involves. [17] 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). This route of nitrogen catabolism allows these animals to conserve water by excreting crystals of uric acid in paste-like solid form. 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. 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. This reaction is catalyzed by “Purine nucleotide phosphorylase”. Why Proteins are Very Important? The biochemical causes of gout are varied. Xanthine oxidase is present in large amounts in liver, intestinal mucosa, and milk. Man does not have this enzyme so urate is the end product for us. • Mammals other than primates oxidize uric acid further to allantonin . Thus, a reduced concentration of UA could decrease the body's capacity to prevent the actions of peroxynitrite and other free radicals on the various neuronal components [26]. urate. It oxidizes hypoxanthine to xanthine and xanthine to uric acid. 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]. ... CMP and UMP are degraded to their respective bases in a series of reactions similar to what we saw in the degradation of purines. 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]. Purine Biosynthesis Purine nucleotide biosynthesis is a complex 10 step process. Lack of urate oxidase in humans results in the final product of the purine degradation pathway being uric acid. 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. Hypoxanthine, xanthine and uric acid are also excreted probably due to the high clearance rate in the blood. [21] identified three mutations in the uricase gene in humans, chimpanzees and gorillas, including two nonsense mutations, one of codon 33 and another of codon 187, and a mutation in the splice acceptor signal of exon 3. It has been suggested that UA, like other purines, is able to stimulate the cerebral cortex and that the superior intellectual power of higher primates may partly be due to these higher levels of UA [44]. 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