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      Protective role of taurine against oxidative stress

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          Abstract

          Taurine is a fundamental mediator of homeostasis that exerts multiple roles to confer protection against oxidant stress. The development of hypertension, muscle/neuro- associated disorders, hepatic cirrhosis, cardiac dysfunction and ischemia/reperfusion are examples of some injuries that are linked with oxidative stress. The present review gives a comprehensive description of all the underlying mechanisms of taurine, with the aim to explain its anti-oxidant actions. Taurine is regarded as a cytoprotective molecule due to its ability to sustain normal electron transport chain, maintain glutathione stores, upregulate anti-oxidant responses, increase membrane stability, eliminate inflammation and prevent calcium accumulation. In parallel, the synergistic effect of taurine with other potential therapeutic modalities in multiple disorders are highlighted. Apart from the results derived from research findings, the current review bridges the gap between bench and bedside, providing mechanistic insights into the biological activity of taurine that supports its potential therapeutic efficacy in clinic. In the future, further clinical studies are required to support the ameliorative effect of taurine against oxidative stress.

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          Most cited references278

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          Organic osmolytes as compatible, metabolic and counteracting cytoprotectants in high osmolarity and other stresses.

          P H Yancey (2005)
          Organic osmolytes are small solutes used by cells of numerous water-stressed organisms and tissues to maintain cell volume. Similar compounds are accumulated by some organisms in anhydrobiotic, thermal and possibly pressure stresses. These solutes are amino acids and derivatives, polyols and sugars, methylamines, methylsulfonium compounds and urea. Except for urea, they are often called ;compatible solutes', a term indicating lack of perturbing effects on cellular macromolecules and implying interchangeability. However, these features may not always exist, for three reasons. First, some of these solutes may have unique protective metabolic roles, such as acting as antioxidants (e.g. polyols, taurine, hypotaurine), providing redox balance (e.g. glycerol) and detoxifying sulfide (hypotaurine in animals at hydrothermal vents and seeps). Second, some of these solutes stabilize macromolecules and counteract perturbants in non-interchangeable ways. Methylamines [e.g. trimethylamine N-oxide (TMAO)] can enhance protein folding and ligand binding and counteract perturbations by urea (e.g. in elasmobranchs and mammalian kidney), inorganic ions, and hydrostatic pressure in deep-sea animals. Trehalose and proline in overwintering insects stabilize membranes at subzero temperatures. Trehalose in insects and yeast, and anionic polyols in microorganisms around hydrothermal vents, can protect proteins from denaturation by high temperatures. Third, stabilizing solutes appear to be used in nature only to counteract perturbants of macromolecules, perhaps because stabilization is detrimental in the absence of perturbation. Some of these solutes have applications in biotechnology, agriculture and medicine, including in vitro rescue of the misfolded protein of cystic fibrosis. However, caution is warranted if high levels cause overstabilization of proteins.
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            Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1.

            Malfolded proteins in the endoplasmic reticulum (ER) induce cellular stress and activate c-Jun amino-terminal kinases (JNKs or SAPKs). Mammalian homologs of yeast IRE1, which activate chaperone genes in response to ER stress, also activated JNK, and IRE1alpha-/- fibroblasts were impaired in JNK activation by ER stress. The cytoplasmic part of IRE1 bound TRAF2, an adaptor protein that couples plasma membrane receptors to JNK activation. Dominant-negative TRAF2 inhibited activation of JNK by IRE1. Activation of JNK by endogenous signals initiated in the ER proceeds by a pathway similar to that initiated by cell surface receptors in response to extracellular signals.
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              Physiological actions of taurine

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                Author and article information

                Journal
                Mol Med Rep
                Mol Med Rep
                Molecular Medicine Reports
                D.A. Spandidos
                1791-2997
                1791-3004
                August 2021
                24 June 2021
                24 June 2021
                : 24
                : 2
                : 605
                Affiliations
                [1 ]National Hellenic Research Foundation, 11635 Athens, Greece
                [2 ]Department of Internal Medicine and Infectious Diseases, University Hospital of Heraklion, 71110 Heraklion, Greece
                [3 ]Department of Molecular Biology and Genetics, Faculty of Health Sciences, Democritus University of Thrace, 68100 Alexandroupolis, Greece
                [4 ]Department of Cancer Genetics, Therapeutics and Ultrastructural Pathology, The Cyprus Institute of Neurology and Genetics, 2371 Nicosia, Cyprus
                [5 ]The Cyprus School of Molecular Medicine, 2371 Nicosia, Cyprus
                [6 ]Department of Internal Medicine and Infectious Diseases, University Hospital of Heraklion, 71110 Heraklion, Greece
                [7 ]Nasco AD Biotechnology Laboratory, 18536 Pireus, Greece
                Author notes
                Correspondence to: Dr Vassilis Zoumpourlis, National Hellenic Research Foundation, 48 Vasileos Konstantinou Avenue, 11635 Athens, Greece, E-mail: vzub@ 123456eie.gr
                Article
                MMR-0-0-12242
                10.3892/mmr.2021.12242
                8240184
                34184084
                bfdf3cdc-d617-4074-b174-18e6d943c76c
                Copyright: © Baliou et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 29 March 2021
                : 03 June 2021
                Funding
                Funded by: The State Scholarships Foundation
                Award ID: 2018-050-0502-13155
                Funded by: European Infrastructure For Translational Medicine-Greece project
                Award ID: MIS 5028091
                Funded by: Operational Program ‘Competitiveness, Entrepreneurship and Innovation’
                Award ID: NSRF 2014-2020
                Funded by: Greece and the European Union (European Regional Development Fund)
                The present study was supported by The State Scholarships Foundation (I.K.Y; grant no. 2018-050-0502-13155). This work was also supported by the European Infrastructure For Translational Medicine-Greece project (grant no. MIS 5028091) which is implemented under the Action ‘Reinforcement of the Research and Innovation Infrastructure’, funded by the Operational Program ‘Competitiveness, Entrepreneurship and Innovation’ (grant no. NSRF 2014-2020) and co-financed by Greece and the European Union (European Regional Development Fund).
                Categories
                Review

                taurine,oxidative stress,therapeutics,neurotoxicity,cardiotoxicity,hepatotoxicity

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