The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform

Ralph Dawson - One of the best experts on this subject based on the ideXlab platform.

  • Attenuation of Oxidative Damage to Dna by Tairome and Taurine Analogs
    Advances in Experimental Medicine and Biology, 2020
    Co-Authors: Steve A. Messina, Ralph Dawson
    Abstract:

    Taurine has been suggested to have cytoprotective actions via a number of different mechanisms. The role of Taurine in protecting DNA from oxidative damage has received only limited attention. The aim of the present studies was to test the hypothesis that Taurine might act to attenuate oxidative damage to DNA caused by free radicals generated by iron-stimulated catecholamine oxidation in the presence of H2O2. Calf thymus DNA (100 μg/tube) was exposed to a reaction mixture containing: ferric chloride (60 μM), H2O2 (2.8 mM) and L-dopa (100 μM).Taurine and Taurine analogs were added simultaneously to determine their effects to prevent oxidative damage to DNA. The reaction was carried out for 1 hour at 37° C and terminated by rapid freezing in an ethanol/dry ice bath. The DNA was precipitated with ethanol and subsequently hydrolyzed with formic acid under vacuum. The hydroxylated bases were separated by HPLC and detected electrochemically. All experiments were replicated a minimum of 5 times. Taurine (20 mM) was found to reduce (p〈0.05) damage to DNA as indexed by reductions in the formation of 5-OH-uracil (49%↓)8-OH adenine (37%↓)and 8-OH guanine (21%↓)Taurine had minimal effects to reduce the formation of 5-OH cytosine (〈7%↓) Taurine (20 mM) also increased total DNA recovery after damage 3640% and increased total undamaged guanine -32%. 5-OH Uracil formation could be reduced (p〈0.05) by 1 mM Taurine and 8-OH-adenine formation was reduced (p〈0.05) by 5 mM Taurine. Studies were conducted with various amino acid analogs and total base adduct formation was reduced by 20 mM β-alanine (30%↓) lysine (58%↓) and glutathione (88%↓) When tested at 20 mM, both hypoTaurine and homoTaurine provided greater protection against DNA damage than Taurine, whereas isethionic acid provided a similar level of protection as Taurine. Using identical conditions as the assays for base hydroxylation, we tested whether inhibition of quinone formation could account for Taurine's mechanism of action. Taurine (49%↓) homoTaurine (24%↓) and hypoTaurine (79%↓) all reduced quinone formation. Thus, inhibition of quinone formation could account for part of Taurines mechanism of action to inhibit oxidative damage, but it could not account for homoTaurine's greater efficacy in preventing DNA damage. Overall, these studies show that Taurine at concentrations normally found in cells can inhibit oxidative damage to DNA.

  • Taurine-induced long-lasting potentiation in the rat hippocampus shows a partial dissociation from total hippocampal Taurine content and independence from activation of known Taurine transporters.
    Journal of Neurochemistry, 2004
    Co-Authors: John E. Dominy, Ralph Dawson, Joanna Peris, J. S. Thinschmidt, Roger L. Papke
    Abstract:

    Perfusion with high millimolar levels of Taurine evoked a longlasting potentiation (LLP-TAU) of synaptic transmission in the Schaffer-collateral CA1 region of the rat hippocampus. Although LLP-TAU showed some correlations to increases in the total Taurine content of hippocampal slices, it could not be blocked by the Taurine transport inhibitor guanidinoethanesulfonic acid (GES), which was able to significantly reduce total slice Taurine uptake. Inhibition of GABA transport by either nipecotic acid or b-guanidinopropionate failed to abolish LLP-TAU and had no significant effect on Taurine uptake. The combination of GES and nipecotic acid also had no significant effect on LLP-TAU. Experiments with transportable structural analogs of Taurine (b-aminoisobutyric acid, homoTaurine, and isethionic acid) suggest that activation of classical Taurine transport pathways does not always yield a robust LLP-TAU. Hippocampal LLP-TAU could be significantly attenuated, however, by pre-incubation with submillimolar levels of Taurine. In summary, the development of LLP-TAU in the rat hippocampus appears to be associated with the intracellular accumulation rather than the activation of known transporters of Taurine, but the precise means of its accumulation remains to be identified.

  • Building Biosynthetic Schools: Reviewing Compartmentation of CNS Taurine Synthesis
    Neurochemical Research, 2004
    Co-Authors: John Dominy, Stephanie Eller, Ralph Dawson
    Abstract:

    Taurine is one of the mammalian brain's most abundant and indispensable amino acids. Considerable strides have been made in understanding Taurine biosynthesis within the brain, but many disputed issues nonetheless remain. Heading the list is the cellular origin of biosynthetically derived Taurine: glial or neuronal? This article reviews the competing theories surrounding cellular compartmentation of Taurine biosynthesis in the brain. It concludes that while in vitro systems clearly show astrocytes to be fully capable of Taurine synthesis and neurons to be limited to synthesizing Taurine from hypoTaurine, there is insufficient evidence to attribute these processes to any one cell type in vivo . Instead, there is a growing body of evidence that suggests brain Taurine biosynthesis is occurring via a more cooperative metabolic interaction between astrocytes and neurons.

  • Taurine inhibition of metal-stimulated catecholamine oxidation
    Neurotoxicity Research, 2000
    Co-Authors: Ralph Dawson, Baerbel Eppler, Debbie Shih, Deron Baker, Elisa Tang, Hunter Hern, Ming Hu
    Abstract:

    Taurine is an abundant amino acid found in mammalian tissues and it has been suggested to have cyto-protective functions. The aim of the present study was to determine if Taurine had the potential to reduce oxidative stress associated with metal-stimulated catecholamine oxidation. Taurine and structural analogs of Taurine were tested for their ability to inhibit metal-stimulated quinone formation from dopamine or L-dopa. Oxidative damage to proteins and lipids were also assessed in vitro and the effects of Taurine were determined. Taurine (20 mM) was found to decrease significantly ferric iron (50–500 μM)- and manganese (10 μM)-stimulated L-dopa or dopamine oxidation. Taurine had no effect on zinc-induced dopamine oxidation and slightly potentiated copper- and NaIO_4-stimulated quinone formation. Ferric iron-stimulated lipid peroxidation was not affected by Taurine (1–20 mM). Protein carbonyl formation induced by ferric iron (500 μM) and L-dopa (500 μM) was significantly reduced by 10 mM Taurine. The cytotoxicity of L-dopa (250 μM) and ferric chloride (75 μM) to LLC-PK_1 cells was attenuated by 10 mM Taurine or hypoTaurine. HomoTaurine alone stimulated L-dopa oxidation and potentiated the cytotoxic effects of ferric iron. HomoTaurine was found to be cytotoxic when combined with L-dopa or L-dopa/iron. In contrast, hypoTaurine inhibited quinone formation and protected LLC-PK_1 cells. These studies suggest that Taurine may exhibit cytoprotective effects against the oxidation products of catecholamines by acting as a scavenger for free radicals and cytotoxic quinones.

  • The effects of Taurine in a rodent model of aging.
    Advances in Experimental Medicine and Biology, 1996
    Co-Authors: Ralph Dawson, Baerbel Eppler, Tucker A. Patterson, Debbie Shih
    Abstract:

    A number of excellent review articles have examined the various physiological roles of Taurine in adult and developing organisms19, 20, 39. A conclusion that can be drawn from these various reviews is that there is a dearth of information on the role of Taurine in aging and senescence. A few studies have examined the tissue content of Taurine in aging animal models. In general Taurine content seems to decline modestly with advanced age. What is unclear is whether the aging process may increase the demand for the protective and regulatory actions of Taurine in cellular homeostasis. This article will briefly review what is known about changes in Taurine content and function during senescence and describe our recent studies of Taurine supplementation using a common rodent model of aging. We will also discuss the potential consequences of a diminished cytoprotective role of Taurine in advanced aging due to a age-related decrement in Taurine homeostasis.

Stephen W Schaffer - One of the best experts on this subject based on the ideXlab platform.

  • Effect of Taurine on Protein Kinase C Isoforms: Role in Taurine’s Actions?
    Advances in Experimental Medicine and Biology, 2020
    Co-Authors: Viktor Pastukh, Junichi Azuma, Viktoriya Solodushko, Stephen W Schaffer
    Abstract:

    Taurine is generally found to be cytoprotective, diminishing damage resulting from ischemia and from initiators of heart failure. Also linked to similar events in the heart is the protein kinase C (PKC) family, which consists of at least 12 different isoforms. Therefore, we proposed that PKC might contribute to the beneficial effects of Taurine on cell viability and growth. One of the PKC isoforms that has been advanced as an important mediator of cytoprotection during ischemia is PKCϵ. In this study, we found that incubation of isolated cardiomyocytes with medium containing 20 mM Taurine led to the translocation ofPKCϵ into the membrane, an event commonly associated with the cardioprotective actions of the PKC isozyme. In addition, Taurine promoted the upregulation of PKCα PKCβ2 and PKCζ. Because the effects of Taurine and angiotensin II on PKC distribution were largely additive, PKC does not appear to contribute to the antagonism between Taurine and angiotensin II. However, the upregulation of PKC by Taurine is consistent with a role of Taurine in normal cell growth. In the Taurine deficient heart, cardiomyocyte size is reduced, an effect that is consistent with the effect of Taurine on PKCϵ. In conclusion, the cytoprotective and pro-growth actions of Taurine appears to be mediated in part by the activation of PKCϵ.

  • effects and mechanisms of Taurine as a therapeutic agent
    Biomolecules & Therapeutics, 2018
    Co-Authors: Stephen W Schaffer
    Abstract:

    Taurine is an abundant, β-amino acid with diverse cytoprotective activity. In some species, Taurine is an essential nutrient but in man it is considered a semi-essential nutrient, although cells lacking Taurine show major pathology. These findings have spurred interest in the potential use of Taurine as a therapeutic agent. The discovery that Taurine is an effective therapy against congestive heart failure led to the study of Taurine as a therapeutic agent against other disease conditions. Today, Taurine has been approved for the treatment of congestive heart failure in Japan and shows promise in the treatment of several other diseases. The present review summarizes studies supporting a role of Taurine in the treatment of diseases of muscle, the central nervous system, and the cardiovascular system. In addition, Taurine is extremely effective in the treatment of the mitochondrial disease, mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and offers a new approach for the treatment of metabolic diseases, such as diabetes, and inflammatory diseases, such as arthritis. The review also addresses the functions of Taurine (regulation of antioxidation, energy metabolism, gene expression, ER stress, neuromodulation, quality control and calcium homeostasis) underlying these therapeutic actions.

  • Physiological roles of Taurine in heart and muscle
    Journal of Biomedical Science, 2010
    Co-Authors: Stephen W Schaffer, Chian Ju Jong, Ramila Kc, Junichi Azuma
    Abstract:

    Taurine (aminoethane sulfonic acid) is an ubiquitous compound, found in very high concentrations in heart and muscle. Although Taurine is classified as an amino acid, it does not participate in peptide bond formation. Nonetheless, the amino group of Taurine is involved in a number of important conjugation reactions as well as in the scavenging of hypochlorous acid. Because Taurine is a fairly inert compound, it is an ideal modulator of basic processes, such as osmotic pressure, cation homeostasis, enzyme activity, receptor regulation, cell development and cell signalling. The present review discusses several physiological functions of Taurine. First, the observation that Taurine depletion leads to the development of a cardiomyopathy indicates a role for Taurine in the maintenance of normal contractile function. Evidence is provided that this function of Taurine is mediated by changes in the activity of key Ca^2+ transporters and the modulation Ca^2+ sensitivity of the myofibrils. Second, in some species, Taurine is an established osmoregulator, however, in mammalian heart the osmoregulatory function of Taurine has recently been questioned. Third, Taurine functions as an indirect regulator of oxidative stress. Although this action of Taurine has been widely discussed, its mechanism of action is unclear. A potential mechanism for the antioxidant activity of Taurine is discussed. Fourth, Taurine stabilizes membranes through direct interactions with phospholipids. However, its inhibition of the enzyme, phospholipid N-methyltransferase, alters the phosphatidylcholine and phosphatidylethanolamine content of membranes, which in turn affects the function of key proteins within the membrane. Finally, Taurine serves as a modulator of protein kinases and phosphatases within the cardiomyocyte. The mechanism of this action has not been studied. Taurine is a chemically simple compound, but it has profound effects on cells. This has led to the suggestion that Taurine is an essential or semi-essential nutrient for many mammals.

  • Renal excretory responses to saline load in the Taurine-depleted and the Taurine-supplemented rat
    Biochemical Pharmacology, 1997
    Co-Authors: Mahmood S. Mozaffari, Junichi Azuma, Champa Patel, Stephen W Schaffer
    Abstract:

    Abstract Taurine is found in high concentrations in mammalian cells. Despite recognition of its role as an organic osmolyte in the kidney, information regarding its effects on renal fluid and electrolyte excretion is sparse. Therefore, the objective of the first series of experiments was to determine the effects of Taurine depletion on renal excretory responses to a saline load. To induce Taurine depletion, male Wistar-Kyoto (WKY) rats were treated with tap water containing 3% β-alanine for 3 weeks. Taurine depletion reduced the initial rates of fluid and sodium excretion after an intravenous saline load. This effect was attributed to Taurine depletion since maintenance of the Taurine-depleted rats on tap water for 2 days to remove the effects of β-alanine yielded the same pattern as the Taurine-depleted rats exposed to β-alanine at the time of the experiment. Nonetheless, rats exposed to short-term β-alanine treatment, which has no influence on kidney Taurine content, demonstrated a larger (~25%) natriuretic but not diuretic response to the isotonic saline load than either the control or Taurine-depleted rats. These data suggest that β-alanine-induced inhibition of tubular reabsorption of Taurine may result in subsequent excretion of Taurine with attendant natriuresis early in the course of β-alanine treatment. We also tested the hypothesis chat Taurine potentiates the renal excretory responses to an isotonic saline load in WKY rats. Inclusion of Taurine in the infusate significantly increased natriuresis and diuresis after a saline load. This effect was greater in animals fed a basal than a high NaCl diet. Our data support a role for Taurine as a natriuretic and diuretic agent.

  • sarcolemmal actions of Taurine linked to altered phospholipid n methylation
    Advances in Experimental Medicine and Biology, 1992
    Co-Authors: Junichi Azumal, Tomoyuki Hamaguchi, Stephen W Schaffer
    Abstract:

    Taurine (2-aminoethanesulfonic acid) is found in very high concentrations in mammalian heart1. There has been numerous studies indicating that Taurine administration attenuates the degree of myocardial injury commonly associated with various models of heart failure2–5. It has been proposed that the mechanism underlying the cardioprotective activity of Taurine relates to its prevention of myocardial calcium overload. The means by which Taurine modulates calcium, however, has not been elucidated. One theory which has been proposed as a unifying hypothesis of Taurine action, suggests that the effects of Taurine are mediated through its interaction with membrane phospholipids. Structurally and chemically many similarities exist between Taurine and the head groups of the neutral phospholipids, such as phosphatidylethanolamine and phosphatidylcholine7. In addition, a fairly linear relationship has been found between the ratio of phosphatidylethanolamine/ phosphatidylcholine in the synaptosomal P2B fraction of developing rat brain and Taurine content8.

Alan R Katritzky - One of the best experts on this subject based on the ideXlab platform.

Masaharu Ukawa - One of the best experts on this subject based on the ideXlab platform.

  • efficacy of Taurine supplementation for preventing green liver syndrome and improving growth performance in yearling red sea bream pagrus major fed low fishmeal diet
    Fisheries Science, 2006
    Co-Authors: Shusaku Takagi, Hisashi Murata, Takanobu Goto, Hideo Hatate, Makoto Endo, Hirofumi Yamashita, Toshiaki Ichiki, Terutoyo Yoshida, Tadashi Sakai, Masaharu Ukawa
    Abstract:

    This study was performed to evaluate the efficacy of Taurine supplementation for preventing green liver syndrome and improving growth performance in red sea bream Pagrus major fed a low-fishmeal (FM) diet. Yearling red sea bream were fed for 34 weeks on low-FM diets either supplemented with Taurine, or without Taurine, and the tissue Taurine and bile pigment concentrations were measured. Compared to the fish fed the FM diet, fish fed the low-FM diet without Taurine supplementation resulted in inferior feed performances and higher incidence of green liver related to the morphological transformation of the erythrocytes. In these fish, the hepatopancreatic Taurine concentration was significantly lower and hepatopancreatic biliverdin concentration was high compared to the fish fed the FM diet. These parameters were markedly improved by Taurine supplementation of the low-FM diet and were similar in levels to the fish fed the FM diet. These results indicate that green liver appearance and inferior feed performances of red sea bream fed the low-FM diet without Taurine supplementation were caused by dietary Taurine deficiency, and indicate the requirement of Taurine supplementation to low-FM diets for red sea bream.

  • hemolytic suppression roles of Taurine in yellowtail seriola quinqueradiata fed non fishmeal diet based on soybean protein
    Fisheries Science, 2006
    Co-Authors: Shusaku Takagi, Hisashi Murata, Takanobu Goto, Masahiro Hayashi, Hideo Hatate, Makoto Endo, Hirofumi Yamashita, Masaharu Ukawa
    Abstract:

    To elucidate the hemolytic suppression roles of Taurine and the necessity of dietary Taurine supplementation in yellowtail Seriola quinqueradiata fed a diet without fishmeal, juvenile fish with an initial body weight of 250 g were fed for 40 weeks in floating net cages on soybean protein diets supplemented with 0, 3.0, 4.5 and 6.0% Taurine. Taurine concentration of the experimental diets were 0.03, 33.9, 52.8 and 71.6 mg/g, respectively. On the 21st week, fish fed the Taurine unsupplemented diet had inferior growth and feed performances, higher death, and there were incidences of green liver and hemolytic anemia. In this group, hepatic and plasma Taurine concentrations, serum osmolality and osmotic tolerance of erythrocytes (EC50 value) were significantly lower, and plasma hydroperoxide concentration was markedly higher than in the Taurine supplemented groups. These conditions markedly improved corresponding with the increase of dietary Taurine concentration. These results indicate that Taurine plays a role in hemolytic suppression through osmoregulation and biomembrane stabilization in fish. In addition, it is suggested that yellowtail requires dietary Taurine as an essential nutrition for maintaining physiological condition normally.

Ruma Banerjee - One of the best experts on this subject based on the ideXlab platform.

  • Taurine biosynthesis by neurons and astrocytes
    Journal of Biological Chemistry, 2011
    Co-Authors: Victor Vitvitsky, Sanjay K Garg, Ruma Banerjee
    Abstract:

    Abstract 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 [35S]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 [35S]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.