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| Taurine (), or 2-aminoethanesulfonic acid, is a non-proteinogenic naturally occurring amino sulfonic acid that is widely distributed in animal tissues. It is a major constituent of bile and can be found in the large intestine, and accounts for up to 0.1% of total human body weight.
Taurine is named after Latin taurus (cognate to Ancient Greek ταῦρος, taûros) meaning bull or ox, as it was first isolated from ox bile in 1827 by German scientists Friedrich Tiedemann and Leopold Gmelin. It was discovered in human bile in 1846 by Edmund Ronalds.
Although taurine is abundant in human organs with diverse putative roles, it is not an essential human dietary nutrient and is not included among nutrients with a recommended intake level. Taurine is synthesized naturally in the human liver from methionine and cysteine.
Taurine is commonly sold as a dietary supplement, but there is no good clinical evidence that taurine supplements provide any benefit to human health. Taurine is used as a food additive for cats (who require it as an essential nutrient), dogs, and poultry.
Taurine concentrations in land plants are low or undetectable, but up to 1000 nmol/g wet weight have been found in algae. |
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Read full article at Wikipedia
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| InChI=1S/C2H7NO3S/c3-1-2-7(4,5)6/h1-3H2,(H,4,5,6) |
| XOAAWQZATWQOTB-UHFFFAOYSA-N |
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Mus musculus
(NCBI:txid10090)
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See:
PubMed
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Saccharomyces cerevisiae
(NCBI:txid4932)
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Source: yeast.sf.net
See:
PubMed
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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DOI
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antioxidant
A substance that opposes oxidation or inhibits reactions brought about by dioxygen or peroxides.
radical scavenger
A role played by a substance that can react readily with, and thereby eliminate, radicals.
Bronsted base
A molecular entity capable of accepting a hydron from a donor (Bronsted acid).
(via organic amino compound )
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Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
Saccharomyces cerevisiae metabolite
Any fungal metabolite produced during a metabolic reaction in Baker's yeast (Saccharomyces cerevisiae ).
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
glycine receptor agonist
An agonist that binds to and activates glycine receptors
nutrient
A nutrient is a food component that an organism uses to survive and grow.
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View more via ChEBI Ontology
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2-aminoethanesulfonic acid
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2-Aminoethanesulfonic acid
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KEGG COMPOUND
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2-aminoethyl sulfonate
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IUBMB
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Aminoethylsulfonic acid
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KEGG COMPOUND
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β-aminoethylsulfonic acid
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NIST Chemistry WebBook
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Taurine
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KEGG COMPOUND
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4486
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DrugCentral
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C00048188
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KNApSAcK
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C00245
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KEGG COMPOUND
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D00047
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KEGG DRUG
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DB01956
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DrugBank
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HMDB0000251
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HMDB
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TAU
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PDBeChem
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Taurine
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Wikipedia
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TAURINE
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MetaCyc
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107-35-7
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CAS Registry Number
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KEGG COMPOUND
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107-35-7
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CAS Registry Number
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NIST Chemistry WebBook
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107-35-7
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CAS Registry Number
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ChemIDplus
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1751215
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Reaxys Registry Number
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Reaxys
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82121
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Gmelin Registry Number
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Gmelin
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Adedara IA, Ojuade TJD, Olabiyi BF, Idris UF, Onibiyo EM, Ajeigbe OF, Farombi EO (2017)
Taurine Ameliorates Renal Oxidative Damage and Thyroid Dysfunction in Rats Chronically Exposed to Fluoride.
Biological trace element research 175, 388-395 [PubMed:27334436]
[show Abstract]
Excessive exposure to fluoride poses several detrimental effects to human health particularly the kidney which is a major organ involved in its elimination from the body. The influence of taurine on fluoride-induced renal toxicity was investigated in a co-exposure paradigm for 45 days using five groups of eight rats each. Group I rats received normal drinking water alone, group II rats were exposed to sodium fluoride (NaF) in drinking water at 15 mg/L alone, group III received taurine alone at a dose of 200 mg/kg group IV rats were co-administered with NaF and taurine (100 mg/kg), while group V rats were co-administered with NaF and taurine (200 mg/kg). Administration of taurine significantly reversed the fluoride-mediated decrease in absolute weight and organo-somatic index of the kidney in the exposed rats. Taurine significantly prevented fluoride-induced elevation in plasma urea and creatinine levels in the exposed rats. Moreover, taurine restored fluoride-mediated decrease in the circulatory concentrations of triiodothyronine, thyroxine, and the ratio of triiodothyronine to thyroxine. Taurine ameliorated fluoride-mediated decrease in renal antioxidant status by significantly enhancing the antioxidant enzyme activities as well as glutathione level in the exposed rats. Additionally, taurine inhibited fluoride-induced renal oxidative damage by markedly decreasing the hydrogen peroxide and malondialdehyde levels as well as improved the kidney architecture in the treated rats. Collectively, taurine protected against fluoride-induced renal toxicity via enhancement of thyroid gland function, renal antioxidant status, and histology in rats. | Hano T, Ito K, Kono K, Ito M, Ohkubo N, Mochida K (2017)
Effect of taurine supplementation on hepatic metabolism and alleviation of cadmium toxicity and bioaccumulation in a marine teleost, red sea bream, Pagrus major.
Fish physiology and biochemistry 43, 137-152 [PubMed:27535560]
[show Abstract]
This study was performed to unravel the mechanism of the beneficial action of taurine on marine teleost fish, red sea bream (Pagrus major), by analyzing the hepatic metabolism. Moreover, the ameliorative effects of the nutrient against cadmium toxicity and bioaccumulation were further evaluated. The fish were fed a diet containing 0 % (TAU0 %), 0.5 % (TAU0.5 %), or 5.0 % (TAU5.0 %) taurine for 40-55 days (d) and subjected to cadmium acute toxicity and bioaccumulation tests. Taurine deficiency in feed severely affected growth and the hepatic metabolic profiles of the fish, including a remarkable increase in myo-inositol, aspartate, and ß-alanine in the TAU0 % group, which indicates a complementary physiological response to taurine deficiency. For the acute toxicity test, fish were fed the test diets for 55 d and were then exposed to different dose of cadmium ranging from 0 to 5.6 mg/L for 96 h. Fish fed taurine had a higher tolerance to cadmium than those not fed taurine. For the bioaccumulation test, fish were fed the test diets for 40 d and then were chronically exposed to 0.2 mg/L of cadmium for 28 d followed by depuration for 21 d. Cadmium concentrations in the liver and muscle of fish fed TAU5.0 % were significantly lower than those of fish fed TAU0 % for the first 7 d of exposure and the first 7 d of elimination. Our findings suggest a possible mechanism for the beneficial role played by taurine and that the inclusion of taurine in fish aquaculture feed may reduce cadmium contamination of fish intended for human consumption. | Ward R, Bridge CA, McNaughton LR, Sparks SA (2016)
The effect of acute taurine ingestion on 4-km time trial performance in trained cyclists.
Amino acids 48, 2581-2587 [PubMed:27380030]
[show Abstract]
Taurine (TAU) has been shown to improve exercise time to exhaustion and 3-km running performance; however, no studies have considered the effect of acute TAU ingestion on short duration cycling time trial (TT) performance. The aim of this study was to determine the effects of a single oral acute dose of 1000 mg of TAU on a laboratory simulated 4-km cycling TT. Eleven trained male cyclists performed three, 4-km TTs. The first of the trials was a familiarisation, followed by two subsequent trials which were performed two hours after the consumption of either 1000 mg of TAU or placebo (P), using a double-blind randomised crossover design. Capillary blood samples were obtained prior to the start and immediately after each TT for the measurement of lactate, pH and HCO3-. There was no effect of TAU (p = 0.731, d = 0.151) on performance (390 ± 27 and 388 ± 21 s for TAU and P, respectively), nor were there any condition main effects for VO2, lactate, pH, or HCO3- (p > 0.05) despite post TT changes in lactate (7.3 ± 2.5 mmol l-1, p < 0.001, d = 2.86, 7.6 ± 2.0 mmol l-1 p < 0.001, d = 3.75); pH (-0.255 ± 0.1, p < 0.001, d = 2.62, -0.258 ± 0.09, p < 0.001, d = 2.87); HCO3- (-13.58 ± 2.7 mmol l-1, p < 0.001, d = 5.04 vs. -13.36 ± 2.3, p < 0.001, d = 5.72 for TAU and P, respectively). The findings of this study suggest that a pre-exercise dose of 1000 mg TAU offers no performance advantage during 4-km TT nor does it alter the blood buffering responses in trained cyclists. | Zhu XY, Ma PS, Wu W, Zhou R, Hao YJ, Niu Y, Sun T, Li YX, Yu JQ (2016)
Neuroprotective actions of taurine on hypoxic-ischemic brain damage in neonatal rats.
Brain research bulletin 124, 295-305 [PubMed:27345710]
[show Abstract]
Taurine is an abundant amino acid in the nervous system, which has been proved to possess antioxidation, osmoregulation and membrane stabilization. Previously it has been demonstrated that taurine exerts ischemic brain injury protective effect. This study was designed to investigate whether the protective effect of taurine has the possibility to be applied to treat neonatal hypoxic-ischemic brain damage. Seven-day-old Sprague-Dawley rats were treated with left carotid artery ligation followed by exposure to 8% oxygen to generate the experimental group. The cerebral damage area was measured after taurine post-treatment with 2,3,5-triphenyltetrazolium chloride (TTC) staining, Hematoxyline-Eosin (HE) staining and Nissl staining. The activities of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), myeloperoxtidase (MPO), ATP and Lactic Acid productions were assayed with ipsilateral hemisphere homogenates. Western-blot and immunofluorescence assay were processed to detect the expressions of AIF, Cyt C, Bax, Bcl-2 in brain. We found that taurine significantly reduced brain infarct volume and ameliorated morphological injury obviously reversed the changes of SOD, MDA, GSH-Px, T-AOC, ATP, MPO, and Lactic Acid levels. Compared with hypoxic-ischemic group, it showed marked reduction of AIF, Cyt C and Bax expressions and increase of Bcl-2 after post-treatment. We conclude that taurine possesses an efficacious neuroprotective effect after cerebral hypoxic-ischemic damage in neonatal rats. | Katakawa M, Fukuda N, Tsunemi A, Mori M, Maruyama T, Matsumoto T, Abe M, Yamori Y (2016)
Taurine and magnesium supplementation enhances the function of endothelial progenitor cells through antioxidation in healthy men and spontaneously hypertensive rats.
Hypertension research : official journal of the Japanese Society of Hypertension 39, 848-856 [PubMed:27412799]
[show Abstract]
Endothelial damage is repaired by endothelial progenitor cells (EPCs), which are pivotal in preventing cardiovascular diseases and prolonging lifespan. The WHO Cardiovascular Diseases and Alimentary Comparison Study demonstrated that dietary taurine and magnesium (Mg) intake suppresses cardiovascular diseases. We herein evaluate the effects of taurine and Mg supplementation on EPC function and oxidative stress in healthy men and spontaneously hypertensive rats (SHRs). Healthy men received taurine (3 g per day) or Mg (340 mg per day) for 2 weeks. SHRs and Wistar-Kyoto (WKY) rats were housed with high-salt drinking water (1% NaCl). The SHRs received 3% taurine solution and/or a high-Mg (600 mg per 100 g) diet for 4 weeks. Their peripheral blood mononuclear cells were separated to quantify EPC colony formation. Oxidative stress markers in their peripheral blood were evaluated using a free radical analytical system and a thiobarbituric acid reactive substance (TBARS) assay. Taurine and Mg supplementation significantly increased EPC colony numbers and significantly decreased free radical levels and TBARS scores in healthy men. Taurine and Mg supplementation significantly increased EPC colony numbers and significantly decreased TBARS scores and free radical levels in SHRs. Nicotinamide adenine dinucleotide phosphate oxidase component mRNA expression was significantly higher in the renal cortex of salt-loaded SHRs than in WKY rats, in which it was suppressed by taurine and Mg supplementation. Taurine and Mg supplementation increased EPC colony formation in healthy men and improved impaired EPC function in SHRs through antioxidation, indicating that the dietary intake of taurine and Mg may prolong lifespan by preventing the progression of cardiovascular diseases. | Rahmeier FL, Zavalhia LS, Tortorelli LS, Huf F, Géa LP, Meurer RT, Machado AC, Gomez R, Fernandes MDC (2016)
The effect of taurine and enriched environment on behaviour, memory and hippocampus of diabetic rats.
Neuroscience letters 630, 84-92 [PubMed:27471162]
[show Abstract]
Diabetes mellitus (DM) has been studied recently as a major cause of cognitive deficits, memory and neurodegenerative damage. Taurine and enriched environment have stood out for presenting neuroprotective and stimulating effects that deserve further study. In this paper, we examined the effects of taurine and enriched environment in the context of diabetes, evaluating effects on behaviour, memory, death and cellular activity. Eighty-eight Wistar rats were divided into 2 groups (E=enriched environment; C=standard housing). Some animals (24/group) underwent induction of diabetes, and within each group, some animals (half of diabetics (D) and half of non-diabetics (ND)/group) were treated for 30days with taurine (T). Untreated animals received saline (S). In total, there were eight subgroups: DTC, DSC, NDTC, NDSC, DTE, DSE, NDTE and NDSE. During the experiment, short-term memory was evaluated. After 30th day of experiment, the animals were euthanized and was made removal of brains used to immunohistochemistry procedures for GFAP and cleaved caspase-3. As a result, we observed that animals treated with taurine showed better performance in behavioural and memory tasks, and the enriched environment had positive effects, especially in non-diabetic animals. Furthermore, taurine and enriched environment seemed to be able to interfere with neuronal apoptosis and loss of glial cells, and in some instances, these two factors seemed to have synergistic effects. From these data, taurine and enriched environment may have important neurostimulant and neuroprotective effects. | Bai J, Yao X, Jiang L, Zhang Q, Guan H, Liu S, Wu W, Qiu T, Gao N, Yang L, Yang G, Sun X (2016)
Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway.
Scientific reports 6, 27733 [PubMed:27291853]
[show Abstract]
Chronic exposures to arsenic had been associated with metabolism diseases. Peroxisome proliferator-activated receptor gamma (PPARγ) was found in the liver, regulated metabolism. Here, we found that the expression of PPARγ was decreased, the generation of reactive oxygen species (ROS) and autophagy were increased after treatment with As2O3 in offsprings' livers. Taurine (Tau), a sulfur-containing β-amino acid could reverse As2O3-inhibited PPARγ. Tau also inhibit the generation of ROS and autophagy. We also found that As2O3 caused autophagic cell death and ROS accelerated in HepG2 cells. Before incubation with As2O3, the cells were pretreated with PPARγ activator Rosiglitazone (RGS), we found that autophagy and ROS was inhibited in HepG2 cells, suggesting that inhibition of PPARγ contributed to As2O3-induced autophagy and the generation of ROS. After pretreatment with Tau, the level of PPARγ was improved and the autophagy and ROS was inhibited in As2O3-treated cells, suggesting that Tau could protect hepatocytes against As2O3 through modulating PPARγ pathway. | Smilowitz JT, O'Sullivan A, Barile D, German JB, Lönnerdal B, Slupsky CM (2013)
The human milk metabolome reveals diverse oligosaccharide profiles.
The Journal of nutrition 143, 1709-1718 [PubMed:24027187]
[show Abstract]
Breast milk delivers nutrition and protection to the developing infant. There has been considerable research on the high-molecular-weight milk components; however, low-molecular-weight metabolites have received less attention. To determine the effect of maternal phenotype and diet on the human milk metabolome, milk collected at day 90 postpartum from 52 healthy women was analyzed by using proton nuclear magnetic resonance spectroscopy. Sixty-five milk metabolites were quantified (mono-, di-, and oligosaccharides; amino acids and derivatives; energy metabolites; fatty acids and associated metabolites; vitamins, nucleotides, and derivatives; and others). The biological variation, represented as the percentage CV of each metabolite, varied widely (4-120%), with several metabolites having low variation (<20%), including lactose, urea, glutamate, myo-inositol, and creatinine. Principal components analysis identified 2 clear groups of participants who were differentiable on the basis of milk oligosaccharide concentration and who were classified as secretors or nonsecretors of fucosyltransferase 2 (FUT2) gene products according to the concentration of 2'-fucosyllactose, lactodifucotetraose, and lacto-N-fucopentaose I. Exploration of the interrelations between the milk sugars by using Spearman rank correlations revealed significant positive and negative associations, including positive correlations between fucose and products of the FUT2 gene and negative correlations between fucose and products of the fucosyltransferase 3 (FUT3) gene. The total concentration of milk oligosaccharides was conserved among participants (%CV = 18%), suggesting tight regulation of total oligosaccharide production; however, concentrations of specific oligosaccharides varied widely between participants (%CV = 30.4-84.3%). The variability in certain milk metabolites suggests possible roles in infant or infant gut microbial development. This trial was registered at clinicaltrials.gov as NCT01817127. | Roux A, Xu Y, Heilier JF, Olivier MF, Ezan E, Tabet JC, Junot C (2012)
Annotation of the human adult urinary metabolome and metabolite identification using ultra high performance liquid chromatography coupled to a linear quadrupole ion trap-Orbitrap mass spectrometer.
Analytical chemistry 84, 6429-6437 [PubMed:22770225]
[show Abstract]
Metabolic profiles of biofluids obtained by atmospheric pressure ionization mass spectrometry-based technologies contain hundreds to thousands of features, most of them remaining unknown or at least not characterized in analytical systems. We report here on the annotation of the human adult urinary metabolome and metabolite identification from electrospray ionization mass spectrometry (ESI-MS)-based metabolomics data sets. Features of biological interest were first of all annotated using the ESI-MS database of the laboratory. They were also grouped, thanks to software tools, and annotated using public databases. Metabolite identification was achieved using two complementary approaches: (i) formal identification by matching chromatographic retention times, mass spectra, and also product ion spectra (if required) of metabolites to be characterized in biological data sets to those of reference compounds and (ii) putative identification from biological data thanks to MS/MS experiments for metabolites not available in our chemical library. By these means, 384 metabolites corresponding to 1484 annotated features (659 in negative ion mode and 825 in positive ion mode) were characterized in human urine samples. Of these metabolites, 192 and 66 were formally and putatively identified, respectively, and 54 are reported in human urine for the first time. These lists of features could be used by other laboratories to annotate their ESI-MS metabolomics data sets. | Le Gall G, Noor SO, Ridgway K, Scovell L, Jamieson C, Johnson IT, Colquhoun IJ, Kemsley EK, Narbad A (2011)
Metabolomics of fecal extracts detects altered metabolic activity of gut microbiota in ulcerative colitis and irritable bowel syndrome.
Journal of proteome research 10, 4208-4218 [PubMed:21761941]
[show Abstract]
(1)H NMR spectroscopy of aqueous fecal extracts has been used to investigate differences in metabolic activity of gut microbiota in patients with ulcerative colitis (UC) (n = 13), irritable bowel syndrome (IBS) (n = 10), and healthy controls (C) (n = 22). Up to four samples per individual were collected over 2 years giving a total of 124 samples. Multivariate discriminant analysis, based on NMR data from all three groups, was able to predict UC and C group membership with good sensitivity and specificity; classification of IBS samples was less successful and could not be used for diagnosis. Trends were detected toward increased taurine and cadaverine levels in UC with increased bile acid and decreased branched chain fatty acids in IBS relative to controls; changes in short chain fatty acids and amino acids were not significant. Previous PCR-denaturing gradient gel electrophoresis (PCR-DGGE) analysis of the same fecal material had shown alterations of the gut microbiota when comparing UC and IBS groups with controls. Hierarchical cluster analysis showed that DGGE profiles from the same individual were stable over time, but NMR spectra were more variable; canonical correlation analysis of NMR and DGGE data partly separated the three groups and revealed a correlation between the gut microbiota profile and metabolite composition. | Condron C, Casey RG, Kehoe S, Toomey D, Creagh T, Bouchier-Hayes DJ (2010)
Taurine modulates neutrophil function but potentiates uropathogenic E. coli infection in the murine bladder.
Urological research 38, 215-222 [PubMed:19940987]
[show Abstract]
Eradication of a urinary tract infection (UTI) appears to be related to a number of innate host defence mechanisms and their interactions with invading bacteria. Recurrent UTIs (rUTIs) pose a difficult problem in that these bacteria use both host and bacterial factors to evade elimination. Neutrophil bactericidal function is depressed, both systemically and in urine, in patients with a history of recurrent UTI. Taurine is a semi-essential amino acid and is successful in preserving neutrophil bactericidal function in urine. Taurine may preserve neutrophil function at the urothelium and thus aid UTI resolution. Adult female (6 weeks old) C57Bl/6 mice were randomised into three groups: a saline gavage only control group, a saline gavage + E. coli group, and a taurine gavage + E. coli group [21 g/70 kg taurine in 0.9% normal saline (N/S) for 5 days]. Whilst taurine gavage pre-treatment resulted in increased serum neutrophils respiratory burst activity, at the urothelial-endothelial interface it caused higher colony forming units in the urine and a higher incidence of E. coli invasion in the bladder wall with no evidence of increased bladder wall neutrophils infiltration on MPO assay of histological assessment. Histologically there was also evidence of reduced bladder inflammation and urothelial cell apoptosis. In conclusion, taurine effectively increases neutrophils activity but given its anti-inflammatory properties, at the expense of decreased urothelial-endothelial activation thus preventing clearance of active E. coli infection in the bladder. Despite the negative results, this study demonstrates the importance of modulating interactions at the urothelial interface. | Guo K, Li L (2009)
Differential 12C-/13C-isotope dansylation labeling and fast liquid chromatography/mass spectrometry for absolute and relative quantification of the metabolome.
Analytical chemistry 81, 3919-3932 [PubMed:19309105]
[show Abstract]
We report a new quantitative metabolome profiling technique based on differential (12)C-/(13)C-isotope dansylation labeling of metabolites, fast liquid chromatography (LC) separation and electrospray ionization Fourier-transform ion cyclotron resonance mass spectrometry (ESI-FTICR MS) detection. An isotope reagent, (13)C-dansyl chloride, can be readily synthesized. This reagent, along with (12)C-dansyl chloride, provides a simple and robust means of labeling metabolites containing primary amine, secondary amine, or phenolic hydroxyl group(s). It is shown that dansylation labeling offers 1-3 orders of magnitude ESI signal enhancement over the underivatized counterparts. Dansylation alters the chromatographic behaviors of polar and ionic metabolites normally not retainable on a reversed phase (RP) column to an extent that they can be retained and separated by RPLC with high efficiency. There is no isotopic effect on RPLC separation of the differential isotope labeled metabolites, and (12)C-/(13)C-labeled isoforms of metabolites are coeluted and detected by MS for precise and accurate quantification and confident metabolite identification. It is demonstrated that, in the analysis of 20 amino acids, a linear response of over 2 orders of magnitude is achieved for relative metabolite quantification with an average relative standard deviation (RSD) of about 5.3% from replicate experiments. A dansylation standard compound library consisting of 121 known amines and phenols has been constructed and is proven to be useful for absolute metabolite quantification and MS-based metabolite identification in biological samples. As an example, the absolute concentrations of 93 metabolites, ranging from 30 nM to 2510 microM, can be determined from a pooled sample of human urines collected in 5 consecutive days labeled with (12)C-dansylation and spiked with the 121 (13)C-dansylated standards. Relative concentration variations of these metabolites in individual urine samples can also be monitored by mixing the (13)C-dansylated pooled urine sample with the (12)C-dansylated individual sample. With a 12 min fast LC separation combined with FTICR MS, 672 metabolites were detected in a human urine sample with each metabolite peak having a signal-to-noise ratio of greater than 20; the identities of most of the metabolites remain to be determined. This work illustrates that dansylation labeling and fast LC/FTICR MS can be a powerful technique for quantitative profiling of at least 672 metabolites in urine samples in 12 min. | Sreekumar A, Poisson LM, Rajendiran TM, Khan AP, Cao Q, Yu J, Laxman B, Mehra R, Lonigro RJ, Li Y, Nyati MK, Ahsan A, Kalyana-Sundaram S, Han B, Cao X, Byun J, Omenn GS, Ghosh D, Pennathur S, Alexander DC, Berger A, Shuster JR, Wei JT, Varambally S, Beecher C, Chinnaiyan AM (2009)
Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression.
Nature 457, 910-914 [PubMed:19212411]
[show Abstract]
Multiple, complex molecular events characterize cancer development and progression. Deciphering the molecular networks that distinguish organ-confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer (42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity. | Anderson CM, Howard A, Walters JR, Ganapathy V, Thwaites DT (2009)
Taurine uptake across the human intestinal brush-border membrane is via two transporters: H+-coupled PAT1 (SLC36A1) and Na+- and Cl(-)-dependent TauT (SLC6A6).
The Journal of physiology 587, 731-744 [PubMed:19074966]
[show Abstract]
Taurine is an essential amino acid in some mammals and is conditionally essential in humans. Taurine is an abundant component of meat and fish-based foods and has been used as an oral supplement in the treatment of disorders such as cystic fibrosis and hypertension. The purpose of this investigation was to identity the relative contributions of the solute transporters involved in taurine uptake across the luminal membrane of human enterocytes. Distinct transport characteristics were revealed following expression of the candidate solute transporters in Xenopus laevis oocytes: PAT1 (SLC36A1) is a H(+)-coupled, pH-dependent, Na(+)- and Cl(-)-independent, low-affinity, high-capacity transporter for taurine and beta-alanine; TauT (SLC6A6) is a Na(+)- and Cl(-)-dependent, high-affinity, low-capacity transporter of taurine and beta-alanine; ATB(0,+) (SLC6A14) is a Na(+)- and Cl(-)-dependent, high-affinity, low-capacity transporter which accepts beta-alanine but not taurine. Taurine uptake across the brush-border membrane of human intestinal Caco-2 cell monolayers showed characteristics of both PAT1- and TauT-mediated transport. Under physiological conditions, Cl(-)-dependent TauT-mediated uptake predominates at low taurine concentrations, whereas at higher concentrations typical of diet, Cl(-)-independent PAT1-mediated uptake is the major absorptive mechanism. Real-time PCR analysis of human duodenal and ileal biopsy samples demonstrates that PAT1, TauT and ATB(0,+) mRNA are expressed in each tissue but to varying degrees. In conclusion, this study is the first to demonstrate both taurine uptake via PAT1 and functional coexpression of PAT1 and TauT at the apical membrane of the human intestinal epithelium. PAT1 may be responsible for bulk taurine uptake during a meal whereas TauT may be important for taurine supply to the intestinal epithelium and for taurine capture between meals. | Liao XB, Zhou XM, Li JM, Yang JF, Tan ZP, Hu ZW, Liu W, Lu Y, Yuan LQ (2008)
Taurine inhibits osteoblastic differentiation of vascular smooth muscle cells via the ERK pathway.
Amino acids 34, 525-530 [PubMed:18060526]
[show Abstract]
Vascular calcification develops within atherosclerotic lesions and results from a process similar to osteogenesis. Taurine is a free beta-amino acid and plays an important physiological role in mammals. We have recently demonstrated that vascular smooth muscle cells (VSMCs) express a functional taurine transporter. To evaluate the possible role of taurine in vascular calcification, we assessed its effects on osteoblastic differentiation of VSMCs in vitro. The results showed that taurine inhibited the beta-glycerophosphate-induced osteoblastic differentiation of VSMCs as evidenced by both the decreasing alkaline phosphate (ALP) activity and expression of the core binding factor alpha1 (Cbfalpha1). Taurine also activated the extracellular signal-regulated protein kinase (ERK) pathway. Inhibition of ERK pathway reversed the effect of taurine on ALP activity and Cbfalpha1 expression. These results suggested that taurine inhibited osteoblastic differentiation of vascular cells via the ERK pathway. | Tang ZQ, Lu YG, Chen L (2008)
Developmental stability of taurine's activation on glycine receptors in cultured neurons of rat auditory cortex.
Neuroscience letters 430, 54-59 [PubMed:17997039]
[show Abstract]
Taurine is an endogenous amino acid that can activate glycine and/or gamma-aminobutyric acid type A (GABA(A)) receptors in the central nervous system. During natural development, taurine's receptor target undergoes a shift from glycine receptors to GABA(A) receptors in cortical neurons. Here, we demonstrate that taurine's receptor target in cortical neurons remains stable during in vitro development. With whole-cell patch-clamp recordings, we found that taurine always activated glycine receptors, rather than GABA(A) receptors, in neurons of rat auditory cortex cultured for 5-22 days. Our results suggest that the functional sensitivity of glycine and GABA(A) receptors to taurine is critically regulated by their developmental environments. | Jia F, Yue M, Chandra D, Keramidas A, Goldstein PA, Homanics GE, Harrison NL (2008)
Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus.
The Journal of neuroscience : the official journal of the Society for Neuroscience 28, 106-115 [PubMed:18171928]
[show Abstract]
Taurine is one of the most abundant free amino acids in the brain. In a number of studies, taurine has been reported to activate glycine receptors (Gly-Rs) at moderate concentrations (> or = 100 microM), and to be a weak agonist at GABA(A) receptors (GABA(A)-Rs), which are usually activated at high concentrations (> or = 1 mM). In this study, we show that taurine reduced the excitability of thalamocortical relay neurons and activated both extrasynaptic GABA(A)-Rs and Gly-Rs in neurons in the mouse ventrobasal (VB) thalamus. Low concentrations of taurine (10-100 microM) decreased neuronal input resistance and firing frequency, and elicited a steady outward current under voltage clamp, but had no effects on fast inhibitory synaptic currents. Currents elicited by 50 microM taurine were abolished by gabazine, insensitive to midazolam, and partially blocked by 20 microM Zn2+, consistent with the pharmacological properties of extrasynaptic GABA(A)-Rs (alpha4beta2delta subtype) involved in tonic inhibition in the thalamus. Tonic inhibition was enhanced by an inhibitor of taurine transport, suggesting that taurine can act as an endogenous activator of these receptors. Taurine-evoked currents were absent in relay neurons from GABA(A)-R alpha4 subunit knock-out mice. The amplitude of the taurine current was larger in neurons from adult mice than juvenile mice. Taurine was a more potent agonist at recombinant alpha4beta2delta GABA(A)-Rs than at alpha1beta2gamma2 GABA(A)-Rs. We conclude that physiological concentrations of taurine can inhibit VB neurons via activation of extrasynaptic GABA(A)-Rs and that taurine may function as an endogenous regulator of excitability and network activity in the thalamus. | Warskulat U, Heller-Stilb B, Oermann E, Zilles K, Haas H, Lang F, Häussinger D (2007)
Phenotype of the taurine transporter knockout mouse.
Methods in enzymology 428, 439-458 [PubMed:17875433]
[show Abstract]
This chapter reports present knowledge on the properties of mice with disrupted gene coding for the taurine transporter (taut-/- mice). Study of those mice unraveled some of the roles of taurine and its membrane transport for the development and maintenance of normal organ functions and morphology. When compared with wild-type controls, taut-/- mice have decreased taurine levels in skeletal and heart muscle by about 98%, in brain, kidney, plasma, and retina by 80 to 90%, and in liver by about 70%. taut-/- mice exhibit a lower body mass as well as a strongly reduced exercise capacity compared with taut+/- and wild-type mice. Furthermore, taut-/- mice show a variety of pathological features, for example, subtle derangement of renal osmoregulation, changes in neuroreceptor expression, and loss of long-term potentiation in the striatum, and they develop clinically relevant age-dependent disorders, for example, visual, auditory, and olfactory dysfunctions, unspecific hepatitis, and liver fibrosis. Taurine-deficient animal models such as acutely dietary-manipulated foxes and cats, pharmacologically induced taurine-deficient rats, and taurine transporter knockout mouse are powerful tools allowing identification of the mechanisms and complexities of diseases mediated by impaired taurine transport and taurine depletion (Chapman et al., 1993; Heller-Stilb et al., 2002; Huxtable, 1992; Lake, 1993; Moise et al., 1991; Novotny et al., 1991; Pion et al., 1987; Timbrell et al., 1995; Warskulat et al., 2004, 2006b). Taurine, which is the most abundant amino acid in many tissues, is normally found in intracellular concentrations of 10 to 70 mmol/kg in mammalian heart, brain, skeletal muscle, liver, and retina (Chapman et al., 1993; Green et al., 1991; Huxable, 1992; Timbrell et al., 1995). These high taurine levels are maintained by an ubiquitous expression of Na(+)-dependent taurine transporter (TAUT) in the plasma membrane (Burg, 1995; Kwon and Handler, 1995; Lang et al., 1998; Liu et al., 1992; Ramamoorthy et al., 1994; Schloss et al., 1994; Smith et al., 1992; Uchida et al., 1992; Vinnakota et al., 1997; Yancey et al., 1975). Taurine is not incorporated into proteins. It is involved in cell volume regulation, neuromodulation, antioxidant defense, protein stabilization, stress responses, and via formation of taurine-chloramine in immunomodulation (Chapman et al., 1993; Green et al., 1991; Huxtable, 1992; Timbrell et al., 1995). On the basis of its functions, taurine may protect cells against various types of injury (Chapman et al., 1993; Green et al., 1991; Huxtable, 1992; Kurz et al., 1998; Park et al., 1995; Stapleton et al., 1998; Timbrell et al., 1995; Welch and Brown, 1996; Wettstein and Häussinger, 1997). In order to examine the multiple taurine functions, murine models have several intrinsic advantages for in vivo research compared to other animal models, including lower cost, maintenance, and rapid reproduction rate. Further, experimental reagents for cellular and molecular studies are widely available for the mouse. In particular, mice can be easily genetically manipulated by making transgene and knockout mice. This chapter focuses on the phenotype of the TAUT-deficient murine model (taut-/-; Heller-Stilb et al., 2002), which may help researchers elucidate the diverse roles of taurine in development and maintenance of normal organ functions and morphology. | Warskulat U, Andrée B, Lüsebrink J, Köhrer K, Häussinger D (2006)
Switch from actin alpha1 to alpha2 expression and upregulation of biomarkers for pressure overload and cardiac hypertrophy in taurine-deficient mouse heart.
Biological chemistry 387, 1449-1454 [PubMed:17081118]
[show Abstract]
Taurine is the most abundant free amino acid in heart muscle and protects against heart failure. In the present study, the consequences of hereditary taurine deficiency on cardiac gene expression were examined in 2- and 15-16-month-old taurine transporter knockout (taut(-/-)) mice using a mouse-specific DNA microarray. This oligonucleotide-based microarray contains probes for 251 genes with relevance for heart function. Of these, 163 probes exhibited a reproducible hybridization signal and were analyzed. alpha-Actin type 1 mRNA levels were 70% lower in the heart of young and older taut(-/-) mice compared to wild-type controls. Interestingly, the hearts of taut(-/-) mice showed a switch from alpha-actin 1 to alpha-actin 2 expression, as confirmed by real-time PCR and Western blot analysis. In addition, mRNA levels of biomarkers for pressure overload and hypertension were upregulated in taut(-/-) hearts, i.e., atrial natriuretic factor (+848%), brain natriuretic peptide (+90%), cardiac ankyrin repeat protein (+118%), and procollagen 1a1, 1a2 and 3a1 (+40% at least). These results point to a stress situation in the heart of taut(-/-) mice under laboratory conditions, and it can be speculated that taut(-/-) hearts may be even more susceptible to failure in the wild when under exogenous stress. | Franconi F, Loizzo A, Ghirlanda G, Seghieri G (2006)
Taurine supplementation and diabetes mellitus.
Current opinion in clinical nutrition and metabolic care 9, 32-36 [PubMed:16444816]
[show Abstract]
Purpose of reviewTaurine is a semi-essential sulphur amino acid derived from methionine and cysteine metabolism. It has been evaluated either in experimental or clinical type 1 and 2 diabetes mellitus and insulin resistance. One form of experiment has included the possibility that perinatal taurine administration could prevent diabetes mellitus and/or insulin resistance.Recent findingsExperimental data suggest strongly that taurine could have beneficial effects in type 1 diabetes mellitus, and could generally reduce organ lipid peroxidation and plasma lipids. Interestingly, retina, lens and nerves seem to respond better to taurine than other organs such as kidneys. It has been shown in some experimental models that in type 2 diabetes mellitus and insulin resistance there is alteration in taurine homeostasis. Taurine could prevent the onset of diabetes mellitus in NOD mice and postnatal taurine modifies the glucose-loading curves in adults. However, the clinical studies are too small and too short to have any real significance.SummaryFurther experimental and clinical studies are required to evaluate taurine's possible therapeutic potential. Careful attention has to be paid in the selection of animal species, in standardization of taurine concentrations and patient selection. Moreover, care must also be given to the metabolic state, presence of complications, duration of supplementations and selection of the right end-points. | Bouckenooghe T, Remacle C, Reusens B (2006)
Is taurine a functional nutrient?
Current opinion in clinical nutrition and metabolic care 9, 728-733 [PubMed:17053427]
[show Abstract]
Purpose of reviewTaurine, a free amino acid, is found in millimolar concentrations in most mammalian tissues. Mammals are able to synthesize taurine endogenously, but some species such as humans are more dependent on dietary sources of taurine. A growing body of evidence suggests that taurine plays a preponderant role in many physiological processes, which will be summarized in this review.Recent findingsEvidence for the requirement of taurine in the human diet has been obtained in many studies involving animal models and a few clinical trials. Recent and past studies suggested that taurine might be a pertinent candidate for use as a nutritional supplement to protect against oxidative stress, neurodegenerative diseases or atherosclerosis. Taurine has demonstrated promising actions in vitro, and as a result clinical trials have begun to investigate its effects on various diseases.SummaryTaurine appears to have multiple functions and plays an important role in many physiological processes, such as osmoregulation, immunomodulation and bile salt formation. Taurine analogues/derivatives have recently been reported to have a marked activity on various disorders. Taken together, these observations actualize the old story of taurine. | Schneider SM, Joly F, Gehrardt MF, Badran AM, Myara A, Thuillier F, Coudray-Lucas C, Cynober L, Trivin F, Messing B (2006)
Taurine status and response to intravenous taurine supplementation in adults with short-bowel syndrome undergoing long-term parenteral nutrition: a pilot study.
The British journal of nutrition 96, 365-370 [PubMed:16923232]
[show Abstract]
Taurine deficiency in patients on long-term parenteral nutrition may be involved in cholestasis. We aimed to assess plasma taurine and tauro-conjugated bile acids in adults with short-bowel syndrome and their response to intravenous taurine. Thirty-two adult patients, who had been on taurine-free parenteral nutrition for a mean of 59 (SE 14) months for short-bowel syndrome, were studied retrospectively. In a second study, a subgroup of ten patients with chronic cholestasis received taurine-enriched (6.0 (SE 0.6) mg/kg per d) parenteral nutrition for 55 (SE 13) months. Post-absorptive plasma taurine and bile acid concentrations were measured and liver function tests routinely sampled. At baseline, plasma taurine was lower in patients with a jejunal length of less than 35 cm (group A, n 16) than in those with a jejunal length of 35 cm or more (group B, n 16): 43 (SE 3) v. 58 (SE 4) micromol/l (P=0.01). The groups were no different in terms of chronic cholestasis (12/16 v.13/16 patients), total bile acids (26 (SE 13) v.14 (SE 5) micromol/l) or the ratio of tauro-conjugated:glyco-conjugated bile acids (5 (SE 2) v.8(SE 4)%, usual range 30-60%). After supplementation, there was an increase in plasma taurine level (63 (SE 8) v. 43 (SE 4), P=0.007) but was no change in either total bile acids or the ratio of tauro-conjugated: glyco-conjugated bile acids. There was a significant decrease in aspartate aminotransferase level. Long-term parenteral nutrition for short-bowel syndrome is associated with an impaired tauro-conjugation of bile acids (enterohepatic pool), irrespective of plasma taurine level (systemic pool) and despite long-term taurine intravenous supplementation. | Kim JW, Kim C (2005)
Inhibition of LPS-induced NO production by taurine chloramine in macrophages is mediated though Ras-ERK-NF-kappaB.
Biochemical pharmacology 70, 1352-1360 [PubMed:16169526]
[show Abstract]
Taurine is an abundant free amino acid in inflammatory cells that protects cells from inflammatory damages. Although the protection mechanism remains unclear, taurine chloramine (Tau-Cl) produced by the reaction between taurine and hypochlorous acid in neutrophils plays an important role. In this study, we investigated the mechanism(s) by which Tau-Cl inhibits LPS-induced NO production in macrophages. Tau-Cl inhibited LPS-induced iNOS expression and NO production in RAW 264.7 cells. LPS treatment elevated the level of active Ras-GTP, and Tau-Cl inhibited LPS-induced Ras activation. Tau-Cl also inhibited ERK1/2 activation in a dose-dependent manner in both RAW 264.7 cells and murine peritoneal macrophages, whereas it did not exert any effect on p38 MAPK activation. Furthermore, Tau-Cl inhibited NF-kappaB activation without affecting AP-1 activity. These results suggest that Tau-Cl suppresses LPS-induced NO production by inhibiting specific signaling pathways. Thus, Tau-Cl protects cells from inflammatory injury resulting from overproduction of NO in a signaling pathway-specific manner. | Peng CT, Wu KH, Lan SJ, Tsai JJ, Tsai FJ, Tsai CH (2005)
Amino acid concentrations in cerebrospinal fluid in children with acute lymphoblastic leukemia undergoing chemotherapy.
European journal of cancer (Oxford, England : 1990) 41, 1158-1163 [PubMed:15911239]
[show Abstract]
Cerebrospinal fluid (CSF) amino acid concentrations were measured in 45 children with acute lymphoblastic leukemia (ALL). Central nervous system (CNS) disease was absent in 34 and present in 11 (Groups L and M, respectively) at diagnosis. Thirty-two otherwise healthy children with febrile convulsions were studied for comparison. Results from this study show that glutamine levels at Day 0 were significantly higher in patients than in controls. Patients in Group M had elevated glutamine levels compared to Group L. In comparison, at Day 14, concentrations of glutamine and asparagine decreased, while glutamic acid amounts increased significantly in Group L. Glutamine levels fell at Day 42 in Group M, which may have resulted from more intensive treatment. From this study we hypothesise that higher baseline glutamine levels are indicative of a greater risk for CNS leukemia. Large-scale prospective trials are required to confirm increased baseline CSF glutamine levels in ALL patients, to identify glutamine as a marker for CNS disease and to clarify underlying mechanisms regulating glutamine in ALL. | Khan SA, Cox IJ, Hamilton G, Thomas HC, Taylor-Robinson SD (2005)
In vivo and in vitro nuclear magnetic resonance spectroscopy as a tool for investigating hepatobiliary disease: a review of H and P MRS applications.
Liver international : official journal of the International Association for the Study of the Liver 25, 273-281 [PubMed:15780050]
[show Abstract]
Nuclear magnetic resonance (NMR) spectroscopy is a non-invasive technique, which allows the study of cellular biochemistry and metabolism. It is a diverse research tool, widely used by biochemists to investigate pathophysiological processes in vitro and, more recently, by physicians to determine disease abnormalities in vivo. This article reviews the basics of the NMR phenomenon and summarises previous research on the hepatobiliary system using both laboratory-based and clinical methodologies. The role of proton and phosphorus-31 ((31)P) NMR spectroscopy in the study of malignant and non-malignant liver disease and studies of bile composition are discussed. In vivo techniques (magnetic resonance spectroscopy, MRS) can be performed as an adjunct to standard MR examination of the liver. Although still primarily a research tool, the in vivo technique provides non-invasive biochemical information on disease severity and holds promise in its use to gauge response to treatment regimens. | Kaplan B, Dinçer S, Babül A, Duyar I (2004)
The effect of taurine administration on vitamin C levels of several tissues in mice.
Amino acids 27, 225-228 [PubMed:15503229]
[show Abstract]
Taurine (2-aminoethane sulphonic acid), a sulphur-containing beta amino acid, is the most prevalent free intracellular amino acid in many human and animal tissues. Vitamin C metabolism is also fluenced by sulphur-containing amino acids. The aim of this study is to investigate the effect of taurine administration on the vitamin C levels of plasma and several tissues (brain, liver, kidneys) in mice with incisional skin wounds. Animals were divided into two as control and taurine groups. Taurine was freshly dissolved in sterile saline and administered daily (60 microl, ip) for five days in the taurine group. At the end of the fifth day, the animals were killed by decapitation. The brain, liver and kidneys were immediately removed. Vitamin C levels were measured in plasma and several tissues. The administration of taurine had no effect on the plasma vitamin C levels (P>0.05) but significantly increased in liver and kidneys (P<0.001). In conclusion, taurine may affect the vitamin C metabolism in tissues by different mechanisms. | Rainesalo S, Keränen T, Palmio J, Peltola J, Oja SS, Saransaari P (2004)
Plasma and cerebrospinal fluid amino acids in epileptic patients.
Neurochemical research 29, 319-324 [PubMed:14992292]
[show Abstract]
Altered plasma and cerebrospinal fluid amino acid levels may be associated with human epilepsy. We studied three groups of patients, those with a generalized epileptic syndrome, juvenile myoclonic epilepsy, patients with refractory localization-related epilepsies, and patients with acute seizures (within 24 h). Plasma levels of amino acids were studied in all patient groups, as were those in the cerebrospinal fluid (CSF) of patients with acute seizures. After acute seizures, the amino acid changes in the CSF were limited to a reduction in the level of taurine, whereas the levels of most amino acids in plasma were decreased. On the other hand, levels of the excitatory amino acids glutamate and aspartate were increased. The most notable finding in the juvenile myoclonic epilepsy patients was an increase in glutamate level in the plasma. Our study supports the conception of an altered metabolism of glutamate in generalized epilepsies. | Engelborghs S, Marescau B, De Deyn PP (2003)
Amino acids and biogenic amines in cerebrospinal fluid of patients with Parkinson's disease.
Neurochemical research 28, 1145-1150 [PubMed:12834252]
[show Abstract]
To study changes in amino acid metabolism and biogenic amines in Parkinson's disease, we set up a prospective study and measured biogenic amines, their main metabolites, and 22 different amino acids, in cerebrospinal fluid of Parkinson's disease patients (n = 24) and age-matched controls (n = 30). A trend toward higher dopamine levels in Parkinson's disease patients was interpreted as an effect of treatment with levodopa and/or selegiline. Significantly lower concentrations of the dopamine metabolite 3,4-dihydroxyphenylacetic acid in the Parkinson's disease group might reflect dopaminergic cell loss. Our results revealed decreased serotonin catabolism that was interpreted as an effect of treatment with selegiline. Whereas all amino acid levels were unchanged, taurine was significantly lower in Parkinson's disease patients. Studies showed that taurine exerts a trophic action on the central nervous system. In this view, decreased taurine in a neurodegenerative disorder as Parkinson's disease deserves attention. | Boelens PG, Houdijk AP, de Thouars HN, Teerlink T, van Engeland MI, Haarman HJ, van Leeuwen PA (2003)
Plasma taurine concentrations increase after enteral glutamine supplementation in trauma patients and stressed rats.
The American journal of clinical nutrition 77, 250-256 [PubMed:12499349]
[show Abstract]
BackgroundTaurine is a unique amino acid with antioxidant and osmolytic properties. Glutamine serves as the preferred fuel for the gut, liver, and immune cells and as a precursor for antioxidants. Trauma patients have low glutamine concentrations.ObjectivesWe investigated the effect of glutamine-enriched enteral nutrition on plasma taurine concentrations in patients with severe trauma (injury severity score >20). Additionally, plasma taurine concentrations and organ fluxes were studied in a stressed rat model.DesignTwenty-nine patients with multiple trauma received glutamine-enriched nutrition and 31 patients received isocaloric, isonitrogenous control solution for 5 d. Plasma taurine and glutamine concentrations were measured. Male Wistar rats (250-300 g) received a glutamine-enriched diet (12%, by wt) or a control solution for 2 wk. Plasma taurine concentrations were measured. Taurine fluxes and fractional extraction rates in the liver, kidneys, and gut were assessed with a radioactive microsphere technique.ResultsBoth patient groups had low taurine concentrations on day 1. From day 3 onward, the glutamine-fed patients had significantly higher taurine concentrations. Rats fed a glutamine-enriched diet had significantly higher plasma taurine concentrations than did the controls. A high taurine uptake was found in the liver, kidneys, and gut of the glutamine-fed rats. Fractional extraction rates were not significantly different between the rat groups.ConclusionsGlutamine enrichment increases plasma taurine in trauma patients and in stressed rats. Because of increased availability, organ fluxes showed a higher taurine uptake in the liver, kidneys, and gut. The reduction in morbidity with glutamine enrichment could be explained in part by increased taurine availability. | Eppler B, Dawson R (2002)
Cytoprotective role of taurine in a renal epithelial cell culture model.
Biochemical pharmacology 63, 1051-1060 [PubMed:11931837]
[show Abstract]
Taurine (TAU) is a sulfur-containing amino acid that has been shown to decrease during aging and is believed to be important for cytoprotection. A decrease in TAU could exacerbate the accumulation of free radical-induced damage that may lead to cell death during the aging process. We have shown previously that TAU directly inhibits dopamine (DA) and (-)-3-(3,4-dihydroxyphenyl)-L-alanine (L-dopa) oxidation. Experiments were conducted to establish a cytoprotective role for TAU. Porcine renal epithelial cells were treated for 1 hr with iron and catecholamines (L-dopa and DA) to produce cytotoxicity by a free radical and quinone mechanism in the absence and presence of 10 or 20mM TAU. Viability assays, protein, and DNA measurements were performed after a 24hr recovery period. In some experiments, cells were extracted immediately after the insult for DA and TAU content measurements using high performance liquid chromatography with electrochemical detection. Catecholamine-induced cytotoxicity caused a 50% loss in cell viability, and 10 or 20mM TAU provided significant protection from cytotoxicity and maintained the functional integrity of the cells. Photomicrographs showed attenuation in cell loss and swelling in the presence of TAU. Pretreatment with 1mM TAU followed by exposure to iron and L-dopa in the presence of 1mM TAU caused a moderate but non-significant increase in cell survival. These data conclusively show that TAU can play a cytoprotective role in the LLC-PK(1) cell culture model. | Cynober LA (2002)
Plasma amino acid levels with a note on membrane transport: characteristics, regulation, and metabolic significance.
Nutrition (Burbank, Los Angeles County, Calif.) 18, 761-766 [PubMed:12297216]
[show Abstract]
The plasma concentration of an amino acid (AA) is the result of its rates of appearance (Ra) in and disappearance (Rd) from plasma. As for most nutrients, AA Ra and Rd are tightly regulated and at the postabsorptive state Ra equals Rd. Factors controlling Ra are protein intake and tissue release; those controlling Rd are tissue uptake and body losses (urine, sweat, etc.). Regulation of plasma AA concentrations involves hormones, in particular insulin and glucagon, both of which induce hypoaminoacidemia (but for quite different reasons), and cortisol, which induces hyperaminoacidemia. In addition, in pathologic states, catecholamines, thyroid hormones, and cytokines modulate plasma AA levels. Peripheral availability of AAs after protein ingestion is controlled by the liver, with an activation of ureagenesis in hyperprotein feeding and repression during a hypoprotein diet. The arginine-to-citrulline pathway in the intestine plays a key role in this adaptative process. In some circumstances tissue uptake of AAs and further metabolism depend on plasma AA concentrations. Plasma glutamine level may be the driving force controlling the flux of this AA at the muscle level. Also, channeling of the arginine cellular pathways means that plasma arginine is a major controlling component of nitric oxide synthesis in endothelial and immune cells. All these features explain the excessive increase in glutamine and arginine demands, in particular for energy expenditure, leading to morbidity (e.g., gut atrophy, muscle wasting, and immune dysfunction) in stressed patients. Normoaminoacidemia is not synonymous with health because this state is observed in level 2 starvation (Ra and Rd decrease) or after minor injury (Ra and Rd increase). Hyperaminoacidemia may be the consequence of organ failure (Rd decreases) or excessive AA intake during parenteral nutrition (Ra increases). Hypoaminoacidemia is observed after organ removal (Ra decreases, e.g., decrease in citrulline concentration in short bowel syndrome) or in stress situations (Rd increases). Mere determinations of plasma AA concentrations at the basal state (i.e., postabsorptive) provide rather limited information. Their usefulness can be improved by measuring arteriovenous differences or performing time course measurements, but techniques based on stable isotopes are necessary to obtain more precise information on the behavior of a particular AA or group of AAs. | Miglis M, Wilder D, Reid T, Bakaltcheva I (2002)
Effect of taurine on platelets and the plasma coagulation system.
Platelets 13, 5-10 [PubMed:11918831]
[show Abstract]
It is not yet clear what exact mechanisms are at work in hibernating animals that prevent clot formation and maintain tissue perfusion under conditions of very slow blood flow and increased blood viscosity brought about by the low temperatures. It has been shown that the total amino acid pool increases more then two fold in hibernating animals with taurine accounting for about 50% of this increase [Storey et al., Proc Natl Acad Sci USA 1988; 85(21): 8350-4]. This work investigates the effect of taurine on platelets and the plasma coagulation system. Taurine was added at different concentrations in the range between 5 and 25 mM to donor plasma. Using STA/STA Compact coagulation analyzer the following tests were performed: prothrombin time (PT), activated partial thromboplastin time (APTT), and thrombin time (TT). At the highest concentration tested (25 mM) taurine prolonged TT by 9%. The prolongation was statistically significant but not clinically significant retaining TT within normal limits (16.7-20.7 s). PT and APTT remained unchanged by taurine. The effect of taurine on platelets was assessed by platelet aggregation by thrombin, extent of platelet shape change (ESC) induced by ADP, and thrombelastography. Taurine at 5 mM final concentration inhibited platelet aggregation by 10%. Increasing taurine concentration to 25 mM did not result in a further augmentation of the inhibitory effect. ESC was unaffected by taurine. Clot strength determined by thrombelastography also remained unchanged by taurine. | Gonzalez-Quevedo A, Obregon F, Fernandez R, Santiesteban R, Serrano C, Lima L (2001)
Amino acid levels and ratios in serum and cerebrospinal fluid of patients with optic neuropathy in Cuba.
Nutritional neuroscience 4, 51-62 [PubMed:11842876]
[show Abstract]
Twenty-one amino acids were determined in serum and cerebrospinal fluid of 12 patients with endemic, and in the cerebrospinal fluid of 22 patients with epidemic optic neuropathy. For the endemic patients, there was a decrease in aspartate and taurine in the serum with respect to controls. The ratios aspartate/taurine and taurine/valine were decreased, and glutamate/taurine was increased in the serum. Some of the altered amino acid ratios indicate preponderance of excitatory to inhibitory molecules. The ratio with valine corresponded to the decrease in taurine and the maintenance of valine concentration, an amino acid related to anthropometric parameters. A typical malnutrition pattern was not observed, as the levels of essential amino acids were not significantly modified. In the cerebrospinal fluid there were increases in aspartate, glutamate and threonine, the first two probably indicating a neurodegenerative disorder or some type of metabolic alteration, primary or secondary to the disease. The increase in threonine could be related to lipid metabolism, but it is not clear at present. A wide variety of amino acid ratios were increased in the cerebrospinal fluid of patients with endemic optic neuropathy, mainly pointing to an excitatory condition and some metabolic alterations. In the cerebrospinal fluid of patients with epidemic optic neuropathy there was an increase in aspartate and glutamate, and increase in glutamate/taurine, glutamate/glycine, and gamma-aminobutyric acid/glycine ratios. Interesting differences were also observed between patients from different periods of time, but with the same clinical features, and the modifications of amino acid concentrations in the cerebrospinal fluid, such as glutamine, threonine and tryptophan. The present results indicate a disorder in the metabolism of amino acids, support a specific deficit, especially for taurine, an imbalance between excitatory and inhibitory amino acids, and a possible relation to viral infections. | Egan BM, Chen G, Kelly CJ, Bouchier-Hayes DJ (2001)
Taurine attenuates LPS-induced rolling and adhesion in rat microcirculation.
The Journal of surgical research 95, 85-91 [PubMed:11162030]
[show Abstract]
BackgroundAdhesion of polymorphonuclear leukocytes (PMN) to endothelial cells and subsequent transendothelial migration are an early key events in the inflammatory response and play an important part in the pathogenesis of septic shock, contributing to vascular and tissue injury. Taurine (2-aminoethanesulfonic acid) is a sulphur-containing beta amino acid. It is a known antioxidant, possesses antimicrobial properties, and has previously been shown to be protective to the endothelium both in vivo and in vitro. The aim of this study was to determine if pretreatment with taurinewould attenuate the lipopolysaccharide (LPS)-induced increase in leukocyte-endothelial interactions and microvascular permeability during endotoxemia.Materials and methodsMale Sprague-Dawley rats (300-350 g) were randomized into three groups: (1) Control, (2) LPS, and (3) LPS + Taurine groups. Taurine was administered orally as a 4% solution. Endotoxemia was induced using Escherichia Coli endotoxin (Serotype 0.55 B5)-15 mg/kg via a slow intravenous infusion. Using mesenteric postcapillary venules (28-32-microm diameter) the number of adherent and migrated leukocytes and their rolling velocity were measured by intravital microscopy at baseline and subsequently at 10, 30, 60, and 90 min post administration of LPS.ResultsFollowing administration of LPS there was a reduction in leukocyte rolling velocity at 30, 60 and 90 min. This was accompanied by a significant increase in the number of adherent leukocytes at 10, 30, 60 and 90 min. Transendothelial migration was significantly increased at 90 min. Taurine significantly attenuated the LPS-induced reduction in leukocyte rolling velocity at 10 and 30 min and the number of adherent leukocytes at all time points. Taurine also attenuated the LPS-induced increase in transendothelial migration at 90 min.ConclusionsThese results demonstrate that taurine ameliorates endotoxin-induced leukocyte-endothelial cell interactions associated with sepsis, thereby suggesting that taurine may have a therapeutic role in the preventionof endothelial damage in sepsis. | Axelson M, Ellis E, Mörk B, Garmark K, Abrahamsson A, Björkhem I, Ericzon BG, Einarsson C (2000)
Bile acid synthesis in cultured human hepatocytes: support for an alternative biosynthetic pathway to cholic acid.
Hepatology (Baltimore, Md.) 31, 1305-1312 [PubMed:10827156]
[show Abstract]
The biosynthesis of bile acids by primary cultures of normal human hepatocytes has been investigated. A general and sensitive method for the isolation and analysis of sterols and bile acids was used, based on anion exchange chromatography and gas chromatography-mass spectrometry (GC/MS). Following incubation for 5 days, 8 oxysterols and 8 C(27)- or C(24)-bile acids were identified in media and cells. Cholic and chenodeoxycholic acids conjugated with glycine or taurine were by far the major steroids found, accounting for 70% and 24% of the total, respectively, being consistent with bile acid synthesis in human liver. Small amounts of sulfated 3beta-hydroxy-5-cholenoic acid and 3beta,7alpha-dihydroxy-5beta-cholanoic acid were also detected. Nine steroids were potential bile acid precursors (2% of total), the major precursors being 7alpha, 12alpha-dihydroxy-3-oxo-4-cholenoic acid and its 5beta-reduced form. These 2 and 5 other intermediates formed a complete metabolic sequence from cholesterol to cholic acid (CA). This starts with 7alpha-hydroxylation of cholesterol, followed by oxidation to 7alpha-hydroxy-4-cholesten-3-one and 12alpha-hydroxylation. Notably, 27-hydroxylation of the product 7alpha, 12alpha-dihydroxy-4-cholesten-3-one and further oxidation and cleavage of the side chain precede A-ring reduction. A-Ring reduction may also occur before side-chain cleavage, but after 27-hydroxylation, yielding 3alpha,7alpha, 12alpha-trihydroxy-5beta-cholestanoic acid as an intermediate. The amounts of the intermediates increased in parallel to those of CA during 4 days of incubation. Suppressing 27-hydroxylation with cyclosporin A (CsA) resulted in a 10-fold accumulation of 7alpha, 12alpha-dihydroxy-4-cholesten-3-one and a decrease of the production of CA and its acidic precursors. These results suggest that the observed intermediates reflect an alternative biosynthetic pathway to CA, which may be quantitatively significant in the cells. | Stover JF, Morganti-Kosmann MC, Lenzlinger PM, Stocker R, Kempski OS, Kossmann T (1999)
Glutamate and taurine are increased in ventricular cerebrospinal fluid of severely brain-injured patients.
Journal of neurotrauma 16, 135-142 [PubMed:10098958]
[show Abstract]
Glutamate contributes to secondary brain damage, resulting in cell swelling and brain edema. Under in vitro conditions, increased extracellular levels of the amino acid taurine reflect glutamate-induced osmotic cell swelling. In vivo, increases in cerebrospinal fluid (CSF) taurine could, therefore, unmask glutamate-mediated cytotoxic edema formation and possibly differentiate it from vasogenic edema. To test this hypothesis, ventricular CSF glutamate and taurine levels were measured in 28 severely brain-injured patients on days 1, 5, and 14 after trauma. Posttraumatic changes in CSF amino acids were investigated in regard to extent of tissue damage and alterations in brain edema as estimated by computerized tomography. On day 1, CSF glutamate and taurine levels were significantly increased in patients with subdural or epidural hematomas (8+/-0.8/71+/-12 microM), contusions (21+/-4.1/122+/-18 microM), and generalized brain edema (13+/-3.2/80+/-15 microM) compared to lumbar control CSF (1.3+/-0.1/12+/-1 microM; p < 0.001). CSF amino acids, however, did not reflect edema formation and resolution as estimated by computerized tomography. CSF taurine correlated positively with glutamate, eventually depicting glutamate-induced cell swelling. However, parallel neuronal release of taurine with its inhibitory function cannot be excluded. Thus, the sensitivity of taurine in unmasking cytotoxic edema formation is weakened by the inability in defining its origin and function under the conditions chosen in the present study. Overall, persisting pathologic ventricular CSF glutamate and taurine levels are highly suggestive of ongoing glial and neuronal impairment in humans following severe traumatic brain injury. | Chesney RW, Helms RA, Christensen M, Budreau AM, Han X, Sturman JA (1998)
The role of taurine in infant nutrition.
Advances in experimental medicine and biology 442, 463-476 [PubMed:9635063]
[show Abstract]
The importance of taurine in the diet of pre-term and term infants has not always been clearly understood and is a topic of interest to students of infant nutrition. Recent evidence indicates that it should be considered one of the "conditionally essential" amino acids in infant nutrition. Plasma values for taurine will fall if infants are fed a taurine-free formula or do not have taurine provided in the TPN solution. Urine taurine values also fall, which is indicative of an attempt by the kidney to conserve taurine. The very-low-birth-weight infant, for a variety of reasons involving the maturation of tubular transport function, cannot maximally conserve taurine by enhancing renal reabsorption and, hence, is potentially at greater risk for taurine depletion than larger pre-term or term infants, and certainly more than older children who have taurine in their diet. Taurine has an important role in fat absorption in pre-term and possibly term infants and in children with cystic fibrosis. Because taurine-conjugated bile acids are better emulsifiers of fat than glycine-conjugated bile acids, the dietary (or TPN) intake has a direct influence on absorption of lipids. Taurine supplementation of formulas or TPN solutions could potentially serve to minimize the brain phospholipid fatty acid composition differences between formula-fed and human milk-fed infants. Taurine appears to have a role in infants, children, and even adults receiving most (> 75%) of their calories from TPN solutions in the prevention of granulation of the retina and electroencephalographic changes. Taurine has also been reported to improve maturation of auditory-evoked responses in pre-term infants, although this point is not fully established. Clearly, taurine is an important osmolyte in the brain and the renal medulla. At these locations, it is a primary factor in the cell volume regulatory process, in which brain or renal cells swell or shrink in response to osmolar changes, but return to their previous volume according to the uptake or release of taurine. While there is a dearth of clinical studies in man concerning this volume regulatory response, studies in cats, rats, and dog kidney cells indicate the protective role of taurine in hyperosmolar stress. The infant depleted of taurine may not be able to respond to hyper- or hyponatremic stress without massive changes in neuronal volume, which has obvious clinical significance. The fact that the brain content of taurine is very high at birth and falls with maturation may be a protective feature, or compensation for renal immaturity Defining an amino acid as "conditionally essential" requires that deficiency result in a clinical consequence or consequences which can be reversed by supplementation. In pre-term and term infants, taurine insufficiency results in impaired fat absorption, bile acid secretion, retinal function, and hepatic function, all of which can be reversed by taurine supplementation. Therefore, this small beta-amino acid, taurine, is indeed conditionally essential. | González-Quevedo A, Obregón F, Santiesteban Freixas R, Fernández R, Lima L (1998)
[Amino acids as biochemical markers in epidemic and endemic optic neuropathies].
Revista cubana de medicina tropical 50 Suppl, 241-244 [PubMed:10349454]
[show Abstract]
It was studied the amino acids pattern in serum and cerebrospinal fluid of 12 and 8 patients, respectively, suffering from optic epidemic neuropathy diagnosed between 1995 and 1997 (endemic period). The cerebrospinal fluid of 16 patients diagnosed during the epidemic (1992) was also studied. The analysis of amino acids in serum and cerebrospinal fluid was made by high resolution liquid chromatography with fluorescent detection, previous derivation with orthofthallic aldehyde. As in the previous study, no important deficiencies of the essential amino acids were observed in the serum of the studied patients. Lower concentrations of threonine, aspartic acid and taurine were found in the serum of patients with epidemic optic neuropathy diagnosed in the endemic period. Taurine plays an important role in the structure and function of photoreceptors of the retina. It is synthesized in the necessary amounts in man, so it must be supplied in the diet. As it is only present in food of animal origin, it is considered that the deficiency of taurine may contribute to the development of optic epidemic neuritis in our patients. Samples of cerebrospinal fluid were analyzed during the epidemic and endemic periods and it was observed an increase of the glutamic and aspartic acid in the epidemic period and of glutamic acid during the endemic. The excess of excitotoxic amino acids in the cerebrospinal fluid supports the previous neurocognitive studies that suggested the affection of the central nervous system in these patients. | Hu S, Zhao X, Yin S, Meng J (1997)
[A study on the mechanism of taurine postponing the aging process of human fetal brain neural cells].
Wei sheng yan jiu = Journal of hygiene research 26, 98-101 [PubMed:10325611]
[show Abstract]
The relationship between taurine and aging of brain neural cells was studied by using primary human fetal brain neural cells cultured in serum-free medium. The results indicated that the activity of superoxide dismutase (SOD) was significantly higher in taurine added group than the control group cultured for 6, 9 and 15 days (P < 0.05). With different taurine levels, the SOD activities of 50 mg/L and 200 mg/L taurine groups were significantly higher than the control group cultured for 6 days (P < 0.05). After 3-day culture, the activity of glutathione peroxidase (GSH-Px) in the taurine added group was significantly higher than the control group (P < 0.05). The membrane lipid fluidity of neural cells decreased with time in control group, but was stable in the group treated with taurine. The fluidity was more stable in the groups treated with 50, 200 and 400 mg/L groups cultured for 6 days, compared with the control group (P < 0.05 or 0.01). The present study showed that taurine is necessary for maintaining membrane lipid fluidity of neural cells in proper levels, and plays an important role in postponing the aging process of brain neural cells. | McMahon GP, O'Kennedy R, Kelly MT (1996)
High-performance liquid chromatographic determination of taurine in human plasma using pre-column extraction and derivatization.
Journal of pharmaceutical and biomedical analysis 14, 1287-1294 [PubMed:8818047]
[show Abstract]
Plasma samples (100 microliters) were treated with 150 microliters of acetonitrile and centrifuged at 5800 g for 10 min and 50 microliters of 10 mM borate buffer (pH 9.2) were added to the supernatant solution. This was followed by the addition of a 50 microliters aliquot of 5 mM fluorescamine in acetonitrile and immediate vortex mixing. A 20 microliters sample was injected on to a reversed-phase HPLC system using a Bondclone C-18 10 microns analytical column (300 mm x 3.9 mm). The mobile phase was tetrahydrofuran-acetonitrile-phosphate buffer (15 mM, pH 3.5) (4:24:72, v/v/v). The taurine derivative was detected by measuring the UV absorbance of 385 nm. Platelet-poor plasma samples were spiked with known amounts of taurine and inter- and intra-assay calibration curves were obtained. The method was applied to the determination of taurine in platelet-rich plasma. | McCarty MF (1996)
Complementary vascular-protective actions of magnesium and taurine: a rationale for magnesium taurate.
Medical hypotheses 46, 89-100 [PubMed:8692051]
[show Abstract]
By a variety of mechanisms, magnesium functions both intracellularly and extracellularly to minimize the cytoplasmic free calcium level, [Ca2+]i. This may be the chief reason why correction of magnesium deficiency, or induction of hypermagnesemia by parenteral infusion, exerts antihypertensive, anti-atherosclerotic, anti-arrhythmic and antithrombotic effects. Although the amino acid taurine can increase systolic calcium transients in cardiac cells (and thus has positive inotropic activity), it has other actions which tend to reduce [Ca2+]i. Indeed, in animal or clinical studies, taurine lowers elevated blood pressure, retards cholesterol-induced atherogenesis, prevents arrhythmias and stabilizes platelets--effects parallel to those of magnesium. The complex magnesium taurate may thus have considerable potential as a vascular-protective nutritional supplement, and might also be administered parenterally, as an alternative to magnesium sulfate, in the treatment of acute myocardial infarction as well as of pre-eclampsia. The effects of magnesium taurate in diabetes deserve particular attention, since both magnesium and taurine may improve insulin sensitivity, and also may lessen risk for the micro- and macrovascular complications of diabetes. | Cozzi R, Ricordy R, Bartolini F, Ramadori L, Perticone P, De Salvia R (1995)
Taurine and ellagic acid: two differently-acting natural antioxidants.
Environmental and molecular mutagenesis 26, 248-254 [PubMed:7588651]
[show Abstract]
Naturally occurring antimutagenic compounds are extensively analyzed for their capacity to protect cells from induced damage. We selected two agents, taurine and ellagic acid, treated in the literature as antioxidants, but whose activity is insufficiently known. This paper reports on the ability of these agents to act against damage induced by mitomycin-C and hydrogen peroxide in Chinese hamster ovary cells cultivated in vitro. Cytogenetic and cytofluorimetric analyses were performed. Ellagic acid proved to have more than one mechanism of action, probably as a scavenger of oxygen species produced by H2O2 treatment, and as a protector of the DNA double helix from alkylating agent injury. In our experimental conditions, taurine seems able to scavenge oxygen species. | Learn DB, Fried VA, Thomas EL (1990)
Taurine and hypotaurine content of human leukocytes.
Journal of leukocyte biology 48, 174-182 [PubMed:2370482]
[show Abstract]
Taurine (T) was reported to be at high concentrations in human leukocytes. It was proposed that T is a scavenger for chlorinated oxidants produced by the myeloperoxidase system of monocytes and neutrophils. Hypotaurine (HT) would be a more effective scavenger, and HT could also detoxify products of bromide or iodide oxidation produced by the eosinophil peroxidase system. Methods previously used to measure T in leukocytes might oxidize HT to T or fail to separate T and HT. Therefore, we examined T and HT content, uptake, and biosynthesis in isolated blood cells and cultured tumor cells derived from hematopoietic/lymphoid cells. Platelets and all leukocytes including monocytes, lymphocytes, neutrophils, and eosinophils had high T levels (10-20 mM), and all except eosinophils had substantial HT levels (0.3-1 mM). Intracellular levels were 500-times higher than in plasma. Erythrocytes were the only blood cells with low levels of both T and HT. Tumor cells from lymphoid (CCRF-CEM) and myeloid (HL-60, K-562, RWLeu4, HEL) lineages took up and concentrated T and HT from the bovine calf serum in the culture medium, and intracellular levels were similar to those in leukocytes. When cells were cultured in HT-supplemented media, HT almost completely replaced T, and HT was not converted to T. Levels of T were not raised by culturing cells with possible precursors, but HT levels were raised when cysteine sulfinic acid was present. Washed tumor cells took up T and HT by way of a beta-amino acid transport system, but uptake by leukocytes was very low. Therefore, leukocytes may acquire T and HT by active uptake rather than biosynthesis, and uptake may be completed during differentiation in the bone marrow. Though HT is low relative to T, HT levels may be sufficient to protect leukocytes from toxic oxidants. | Kopple JD, Vinton NE, Laidlaw SA, Ament ME (1990)
Effect of intravenous taurine supplementation on plasma, blood cell, and urine taurine concentrations in adults undergoing long-term parenteral nutrition.
The American journal of clinical nutrition 52, 846-853 [PubMed:2122710]
[show Abstract]
Thirty-four adults undergoing long-term parenteral nutrition (TPN) were treated either with or without intravenous taurine for less than or equal to 24 mo. Statistical comparisons were carried out in eight patients randomly assigned to receive intravenous taurine, usually 10 mg.kg-1.d-1, and 10 patients not receiving taurine. Compared with normal adults, baseline plasma taurine and urine taurine-creatinine ratios were decreased in both groups and platelet taurine was reduced in the taurine-treated group. During taurine treatment the mean of the mean values for taurine became normal in plasma and platelets and remained normal in erythrocytes, granulocytes, and lymphocytes; urine taurine-creatinine ratios rose to approximately five times normal. During follow-up, patients not given taurine had plasma, erythrocyte, and granulocyte taurine and urine taurine-creatinine ratios below normal values and the concentrations of taurine-treated patients. Their platelet taurine was also subnormal. Thus, 10 mg taurine.kg-1.d-1 intravenously normalizes plasma and blood cell taurine concentrations in long-term TPN patients. | Goodman HO, Shihabi Z, Oles KS (1989)
Antiepileptic drugs and plasma and platelet taurine in epilepsy.
Epilepsia 30, 201-207 [PubMed:2494044]
[show Abstract]
Although older studies have reported elevated plasma taurine concentrations, more recent studies have reported the same or lower plasma taurine concentrations in epileptic than in control subjects. The present study determined plasma taurine concentrations in 114 epileptic and 99 control subjects. In addition, taurine concentrations in platelets, known to be rich in taurine, were assayed. Serum drug concentrations were also determined to detect possible effects on plasma or platelet taurine concentrations. The plasma and platelet taurine concentrations of epileptic subjects were significantly more variable than corresponding control data. Mean platelet taurine was significantly lower for epileptic patients than for controls. Analysis of variance (ANOVA) on data from epileptic patients revealed no significant association between platelet or plasma taurine concentrations and drug or seizure groups. However, t tests revealed a higher mean plasma taurine concentration for patients with primary generalized seizure disorders (group II) receiving valproate (VPA) (p less than 0.004). Utilizing serum drug concentrations, a significant negative correlation (rxy = -0.552) was found between log-converted platelet taurine and serum VPA concentrations (p less than 0.01) among group II patients. Results were interpreted as having potential value for less empiric drug use and as indicating that cellular rather than plasma studies will prove more informative in gaining an understanding of the idiopathic epilepsies. | Sturman JA, Messing JM, Rossi SS, Hofmann AF, Neuringer MD (1988)
Tissue taurine content and conjugated bile acid composition of rhesus monkey infants fed a human infant soy-protein formula with or without taurine supplementation for 3 months.
Neurochemical research 13, 311-316 [PubMed:3393260]
[show Abstract]
The concentrations of taurine in a number of brain regions and in other tissues of rhesus monkeys fed a taurine-free human infant formula for 3 months are substantially lower than in similar monkeys fed the same formula supplemented with taurine. Activities of enzymes involved in taurine biosynthesis were not different in the two groups except for liver cysteinesulfinic acid decarboxylase, which was greater in the monkeys fed formula alone. There was no difference in the biliary bile acid composition, but the proportion of bile acids conjugated with taurine was significantly greater in the monkeys fed formula supplemented with taurine. These results indicate that the effects of a taurine-deficient diet on infant primates are widespread. | Vinton NE, Laidlaw SA, Ament ME, Kopple JD (1987)
Taurine concentrations in plasma, blood cells, and urine of children undergoing long-term total parenteral nutrition.
Pediatric research 21, 399-403 [PubMed:3106924]
[show Abstract]
Taurine concentrations in plasma, platelets, lymphocytes, granulocytes, erythrocytes, and urine were measured in 19 children who were undergoing long-term home parenteral nutrition for 27.4 +/- 7.1 (SEM) months. The parenteral solutions contained methionine, but not taurine or cysteine. The patients' plasma, platelet, and urine taurine concentrations were significantly reduced to 54, 48, and 16%, respectively, of the values from normal children of similar ages. The most significant reductions in plasma and platelet taurine concentrations were observed in the children who were estimated to absorb less than 5% of their daily calorie needs from the enteral tract. Lymphocyte and erythrocyte taurine levels tended to be lower but were not significantly different from those in normal children. The patients' plasma methionine and cystine levels were not different from normal. There was a direct correlation between plasma and platelet taurine concentrations and between plasma and urine taurine. Both plasma and platelet taurine tended to be directly correlated with age and, after the 1st yr of total parenteral nutrition, with the duration of total parenteral nutrition therapy. | Hagenfeldt L, Bjerkenstedt L, Edman G, Sedvall G, Wiesel FA (1984)
Amino acids in plasma and CSF and monoamine metabolites in CSF: interrelationship in healthy subjects.
Journal of neurochemistry 42, 833-837 [PubMed:6198473]
[show Abstract]
Plasma and cerebrospinal fluid (CSF) concentrations of amino acids were measured in 65 healthy volunteers (50 men and 15 women). The CSF levels of the monoamine metabolites homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylethylene glycol (MOPEG), and 5-hydroxyindoleacetic acid (5-HIAA) were also determined. Sex differences were observed in both plasma and CSF amino acid levels as well as in the relationship between these concentrations. No significant correlations were observed between the CSF levels of HVA and 5-HIAA, and the concentrations of their precursor amino acids in either plasma or CSF. The MOPEG level in CSF correlated positively with the plasma concentrations of several amino acids. |
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