Taurine: new implications for an old amino acid

Schuller‐Levis, Georgia; Park, Eunkyue

doi:10.1016/s0378-1097(03)00611-6

Cited by 367 publications

(239 citation statements)

References 47 publications

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“…Taurine can also react directly with a variety of cytotoxic aldehydes, including MDA, suggesting that the protective effects of taurine on heart function may also be related to lowering of aldehyde levels per se. 23 Moreover, we cannot rule out a role of taurine in mediating anti-inflammatory effects, 60 maintaining cellular metabolism (via its effect on mitochondria), 61 and/or protection of coronary endothelium and blood flow. 62 In our murine model, taurine treatment also led to reductions in myocardial iron levels.…”

Section: Oudit Et Almentioning

confidence: 98%

Taurine Supplementation Reduces Oxidative Stress and Improves Cardiovascular Function in an Iron-Overload Murine Model

et al. 2004

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Background-Iron overload has an increasing worldwide prevalence and is associated with significant cardiovascular morbidity and mortality. Elevated iron levels in the myocardium lead to impaired systolic and diastolic function and elevated oxidative stress. Taurine accounts for 25% to 50% of the amino acid pool in myocardium, possesses antioxidant properties, and can inhibit L-type Ca 2ϩ channels. Thus, we hypothesized that this agent would reduce the cardiovascular effects of iron overload. Methods and Results-Iron-overloaded mice were generated by intraperitoneal injection of iron either chronically (5 days per week for 13 weeks) or subacutely (5 days per week for 4 weeks). Iron overload causes increased mortality, elevated oxidative stress, systolic and diastolic dysfunction, hypotension, and bradycardia. Taurine supplementation increased myocardial taurine levels by 45% and led to reductions in mortality and improved cardiac function, heart rate, and blood pressure in iron-overloaded mice. Histological examination of the myocardium revealed reduced apoptosis and interstitial fibrosis in iron-overloaded mice supplemented with taurine. Taurine mediated reduced oxidative stress in iron-overloaded mice along with attenuation of myocardial lipid peroxidation and protection of reduced glutathione level. Conclusions-These results demonstrate that treatment with taurine reduces iron-mediated myocardial oxidative stress, preserves cardiovascular function, and improves survival in iron-overloaded mice. The role of taurine in protecting reduced glutathione levels provides an important mechanism by which oxidative stress-induced myocardial damage can be curtailed. Taurine, as a dietary supplement, represents a potential new therapeutic agent to reduce the cardiovascular burden from iron-overload conditions.

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Section: Oudit Et Almentioning

confidence: 98%

Taurine Supplementation Reduces Oxidative Stress and Improves Cardiovascular Function in an Iron-Overload Murine Model

et al. 2004

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“…Various roles have been ascribed to taurine, including regulation of osmotic pressure (12)(13)(14), neuromodulatory (3,15) and immunomodulatory (16) factors, and as an antioxidant for detoxifying hypochlorous acid, forming taurine chloramine (12). Taurine deficiency is associated with heart dysfunction, brain development abnormalities, retinal degradation, and other pathologies (3,17).…”

mentioning

confidence: 99%

Taurine Biosynthesis by Neurons and Astrocytes

Vitvitsky

Garg

Banerjee

2011

Journal of Biological Chemistry

102

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The physiological roles of taurine, a product of cysteine degradation and one of the most abundant amino acids in the body, remain elusive. Taurine deficiency leads to heart dysfunction, brain development abnormalities, retinal degradation, and other pathologies. The taurine synthetic pathway is proposed to be incomplete in astrocytes and neurons, and metabolic cooperation between these cell types is reportedly needed to complete the pathway. In this study, we analyzed taurine synthesis capability as reported by incorporation of radioactivity from [ 35 S]cysteine into taurine, in primary murine astrocytes and neurons, and in several transformed cell lines (human (SH-SY5Y) and murine (N1E-115) neuroblastoma, human astrocytoma (U-87MG and 1321 N1), and rat glioma (C6)). Extensive incorporation of radioactivity from [35 S]cysteine into taurine was observed in rat glioma cells as well as in primary mouse astrocytes and neurons, establishing the presence of an intact taurine synthesis pathway in these cells. Interestingly, exposure of cells to cysteine or cysteamine resulted in elevated intracellular hypotaurine without a corresponding increase in taurine levels, suggesting that oxidation of hypotaurine limits taurine synthesis in cells. Consistent with its role as an organic osmolyte, taurine synthesis was stimulated under hypertonic conditions in neurons.Taurine, or ethanesulfonic acid, is one of the most abundant amino acids in the body whose physiological role remains elusive. Its biosynthesis involves the sequential oxidation of cysteine to cysteinesulfinic acid, catalyzed by cysteine dioxygenase, decarboxylation by cysteinesulfinate decarboxylase, and oxidation of the resulting hypotaurine to taurine by a putative hypotaurine dehydrogenase (Fig. 1). The latter enzyme has, however, not been purified to homogeneity and remains uncharacterized (1-3). In fact, it has been suggested that oxidation of hypotaurine to taurine might occur via a nonenzymatic reaction in cells (4 -6). Hypotaurine can also be produced via oxidation of cysteamine, the end product of coenzyme A degradation (Fig. 1). Cysteamine oxidation is catalyzed by 2-aminoethanethiol dioxygenase, which is widely expressed in mammalian tissues (7).Although it is generally believed that taurine cannot be further metabolized and is excreted by the kidney or as a bile component, there are several older reports in the literature on the conversion of taurine to isethionic acid in mammalian tissues (8 -11). Various roles have been ascribed to taurine, including regulation of osmotic pressure (12-14), neuromodulatory (3, 15) and immunomodulatory (16) factors, and as an antioxidant for detoxifying hypochlorous acid, forming taurine chloramine (12). Taurine deficiency is associated with heart dysfunction, brain development abnormalities, retinal degradation, and other pathologies (3, 17). Taurine is actively transported into cells by a specific Na ϩ -dependent transporter (TAUT) and accumulates to high concentrations particularly in the liver, muscle, and retina. ...

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“…Several of those newly discovered functions have been tied to taurine conjugation. One reaction involves the detoxification of hypochlorous acid by taurine resulting in the formation of taurine chloramine, a product that has the added benefit of possessing anti-inflammatory activity (Schuller-Levis and Park 2003;Marcinkiewicz and Kontny 2013;Kim and Cha 2014). Taurine also forms a conjugate (5-taurinomethyluridine) with the wobble position uridine of tRNA Leu(UUR) , a reaction that enhances the interaction between the modified uridine and guanine (Kirino et al 2005;Kurata et al 2008;Schaffer et al 2013).…”

Section: Introductionmentioning

confidence: 99%