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      Physiological functions and pathogenic potential of uric acid: A review

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          Graphical abstract

          Uric acid, C 5H 4N 4O 3, 7,9-dihydro-1H-purine-2,6,8(3H)-trione, molecular mass 168 Da, is a product of the metabolic breakdown of purine nucleotides (adenine and guanine).

          Abstract

          Uric acid is synthesized mainly in the liver, intestines and the vascular endothelium as the end product of an exogenous pool of purines, and endogenously from damaged, dying and dead cells, whereby nucleic acids, adenine and guanine, are degraded into uric acid. Mentioning uric acid generates dread because it is the established etiological agent of the severe, acute and chronic inflammatory arthritis, gout and is implicated in the initiation and progress of the metabolic syndrome. Yet, uric acid is the predominant anti-oxidant molecule in plasma and is necessary and sufficient for induction of type 2 immune responses. These properties may explain its protective potential in neurological and infectious diseases, mainly schistosomiasis. The pivotal protective potential of uric acid against blood-borne pathogens and neurological and autoimmune diseases is yet to be established.

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          NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production?

          Jurg Tschopp, Kate Schroder (2010)
          The NLR family, pyrin domain-containing 3 (NLRP3) inflammasome is a multiprotein complex that activates caspase 1, leading to the processing and secretion of the pro-inflammatory cytokines interleukin-1beta (IL-1beta) and IL-18. The NLRP3 inflammasome is activated by a wide range of danger signals that derive not only from microorganisms but also from metabolic dysregulation. It is unclear how these highly varied stress signals can be detected by a single inflammasome. In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS).
          Article 0 comments Cited 671 times – based on 0 reviews     Review now
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            Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis.

            B. N. Ames, R Cathcart, E Schwiers … (1981)
            During primate evolution, a major factor in lengthening life-span and decreasing age-specific cancer rates may have been improved protective mechanisms against oxygen radicals. We propose that one of these protective systems is plasma uric acid, the level of which increased markedly during primate evolution as a consequence of a series of mutations. Uric acid is a powerful antioxidant and is a scavenger of singlet oxygen and radicals. We show that, at physiological concentrations, urate reduces the oxo-heme oxidant formed by peroxide reaction with hemoglobin, protects erythrocyte ghosts against lipid peroxidation, and protects erythrocytes from peroxidative damage leading to lysis. Urate is about as effective an antioxidant as ascorbate in these experiments. Urate is much more easily oxidized than deoxynucleosides by singlet oxygen and is destroyed by hydroxyl radicals at a comparable rate. The plasma urate levels in humans (about 300 microM) is considerably higher than the ascorbate level, making it one of the major antioxidants in humans. Previous work on urate reported in the literature supports our experiments and interpretations, although the findings were not discussed in a physiological context.
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              The NLRP3 inflammasome: a sensor for metabolic danger?

              Kate Schroder, Rongbin Zhou, Jurg Tschopp (2010)
              Interleukin-1beta (IL-1beta), reactive oxygen species (ROS), and thioredoxin-interacting protein (TXNIP) are all implicated in the pathogenesis of type 2 diabetes mellitus (T2DM). Here we review mechanisms directing IL-1beta production and its pathogenic role in islet dysfunction during chronic hyperglycemia. In doing so, we integrate previously disparate disease-driving mechanisms for IL-1beta, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. The NLRP3 inflammasome also drives IL-1beta maturation and secretion in another disease of metabolic dysregulation, gout. Thus, we propose that the NLRP3 inflammasome contributes to the pathogenesis of T2DM and gout by functioning as a sensor for metabolic stress.
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                Author and article information

                Contributors
                Rashika El Ridi
                Journal
                Journal ID (nlm-ta): J Adv Res
                Journal ID (iso-abbrev): J Adv Res
                Title: Journal of Advanced Research
                Publisher: Elsevier
                ISSN (Print): 2090-1232
                ISSN (Electronic): 2090-1224
                Publication date PMC-release: 14 March 2017
                Publication date (Print): September 2017
                Publication date (Electronic): 14 March 2017
                Volume: 8
                Issue: 5
                Pages: 487-493
                Affiliations
                [a ]Zoology Department, Faculty of Science, Cairo University, Giza 12613, Egypt
                [b ]Department of Chemistry, School of Science and Engineering, American University in Cairo, New Cairo 11835, Cairo, Egypt
                Author notes
                Article
                Publisher ID: S2090-1232(17)30034-6
                DOI: 10.1016/j.jare.2017.03.003
                PMC ID: 5512149
                PubMed ID: 28748115
                SO-VID: d400c78a-08e2-41d6-ae2f-5b4861dd62c8
                Copyright © © 2017 Production and hosting by Elsevier B.V. on behalf of Cairo University.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 24 November 2016
                Date revision received : 11 March 2017
                Date accepted : 11 March 2017
                Categories
                Subject: Review

                Keywords: uric acid,type 2 cytokines,arachidonic acid,schistosomiasis vaccine,gout,metabolic syndrome
                Data availability:
                Keywords: uric acid, type 2 cytokines, arachidonic acid, schistosomiasis vaccine, gout, metabolic syndrome

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