Taurine: Biological Update

Wright, Charles E.; Tallan, Harris H.; Lin, Yong Y.; Gaull, Gerald E.

doi:10.1146/annurev.bi.55.070186.002235

Cited by 552 publications

(221 citation statements)

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“…Thus, the cellular origin of taurine release in brain in ALF is still unclear. In addition, ammonia-induced taurine release is not necessarily related to a cell volume regulatory response [33] and [34]. It remains to be determined whether previously reported taurine release into the extracellular space [4] or changes in cerebrospinal fluid (CSF) taurine concentrations [31] are implicated in the pathogenesis of encephalopathy or brain edema in ALF.…”

Section: Discussionmentioning

confidence: 99%

Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia

et al. 2004

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Zwingmann, C. et al., 2004. Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia. Brain Research, 999(1), ABSTRACTThe principal cause of mortality in patients with acute liver failure (ALF) is brain herniation resulting from intracranial hypertension caused by a progressive increase of brain water. In the present study, ex vivo highresolution 1 H-NMR spectroscopy was used to investigate the effects of ALF, with or without superimposed hypothermia, on brain organic osmolyte concentrations in relation to the severity of encephalopathy and brain edema in rats with ALF due to hepatic devascularization. In normothermic ALF rats, glutamine concentrations in frontal cortex increased more than fourfold at precoma stages, i.e. prior to the onset of severe encephalopathy, but showed no further increase at coma stages. In parallel with glutamine accumulation, the brain organic osmolytes myo-inositol and taurine were significantly decreased in frontal cortex to 63% and 67% of control values, respectively, at precoma stages (p<0.01), and to 58% and 67%, respectively, at coma stages of encephalopathy (p<0.01). Hypothermia, which prevented brain edema and encephalopathy in ALF rats, significantly attenuated the depletion of myo-inositol and taurine. Brain glutamine concentrations, on the other hand, did not respond to hypothermia. These findings demonstrate that experimental ALF results in selective changes in brain organic osmolytes as a function of the degree of encephalopathy which are associated with brain edema, and provides a further rationale for the continued use of hypothermia in the management of this condition.

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Section: Discussionmentioning

confidence: 99%

Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia

et al. 2004

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“…On the other hand, taurine, a sulfur-containing ␤-amino acid, is also suggested as having a protective effect against oxidative damage induced by compounds such as carbon tetrachloride (Nakashima et al 1982), bleomycin and paraquat (Gordon et al 1992) and ethanol (Kerai et al 1999). The following mechanisms have been proposed for the antioxidant effects of taurine: (1) As a direct antioxidant, taurine would quench and detoxify some reactive intermediates such as hypochlorous acid generated by myeloperoxidase (Wright et al 1986;Huxtable 1992;Timbrell et al 1995), nitric oxide (Redmond et al 1996), and H 2 O 2 (Cozzi et al 1995). Taurine was also reported to have scavenged HO • , but this scavenging activity has been shown to be weak compared to that of glucose and mannitol (Aruoma et al 1988).…”

Section: Discussionmentioning

confidence: 99%

“…(2) As an indirect antioxidant, taurine may protect cells via intercalating into the membrane and stabilizing it (Nakashima et al 1982;Gordon et al 1992;Timbrell et al 1995). The membrane-protective effect of taurine is suggested to be related to an action on permeability to ions and water (Wright et al 1986;Timbrell et al 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Taurine, a sulfur-containing ␤-amino acid (Figure 1) is found in millimolar concentrations, especially in tissues that are excitable, rich in membranes, and generate oxidants (Jacobsen and Smith 1968;Wright et al 1986). The sulfonate group in taurine is a strong acid that makes it completely zwitterionic over the physiological pH range (Huxtable 1992).…”

mentioning

confidence: 99%

“…The sulfonate group in taurine is a strong acid that makes it completely zwitterionic over the physiological pH range (Huxtable 1992). A number of functions have been shown for taurine, such as maintaining calcium homeostasis, osmoregulation, removal of hypochlorous acid, and stabilizing the membranes (Gaull et al 1985;Wright et al 1986;Huxtable 1992). Some of the recent data indicate that taurine can act as a direct antioxidant by scavenging reactive oxygen species (ROS) (Cozzi et al 1995;Redmond et al 1996) and/or as an indirect antioxidant by preventing changes in membrane permeability due to oxidant injury (Nakashima et al 1982;Banks et al 1992;Gordon et al 1992).…”

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confidence: 99%

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Antioxidant Effect of Taurine Against Lead-Induced Oxidative Stress

Gürer

Özgüneş

Saygın

et al. 2001

Arch. Environ. Contam. Toxicol.

139

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Abstract. Oxidative stress is proposed as a molecular mechanism in lead toxicity, which suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate whether taurine has a beneficial effect both on Chinese hamster ovary (CHO) cells and on Fisher 344 (F344) rats following lead exposure. Therefore, oxidative stress parameters (glutathione, malondialdehyde levels, catalase, and glucose-6-phosphate dehydrogenase [G6PD] activities) of lead-exposed CHO cells and F344 rats were determined following taurine treatment. Taurine was found to be effective in (1) increasing glutathione levels that had been diminished by lead; (2) reducing malondialdehyde levels, an end-product of lipid peroxidation; (3) decreasing catalase and erythrocyte G6PD activity, which had been increased by lead exposure; and (4) improving cell survival of CHO cells. However, taurine had no effect on blood and tissue lead levels when 1.1 g/kg/day taurine was administered to F344 rats for 7 days, following 5 weeks of lead exposure (2,000 ppm lead acetate). As a result, taurine seems to be capable of fortifying cells against lead-induced oxidative attack without decreasing lead levels. Therefore, administration of taurine, accompanied by a chelating agent, might increase its effectiveness in the treatment of lead poisoning.

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Regeneration and myogenic cell proliferation correlate with taurine levels in dystrophin- and MyoD-Deficient muscles

et al. 1998

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This study coupled proton magnetic resonance spectroscopy (1H-NMR) and in situ hybridization plus autoradiography in a novel examination of different phenotypes of adult myogenesis that arise from genetic disruptions in mice. Study of muscle extracts from normal and dystrophin-deficient mdx limb and diaphragm muscles confirmed our previous findings linking taurine and muscle regeneration at the peak of damage and repair. 1H-NMR distinguished biochemical differences in regenerating muscles that were consistent with the extent of repair in three strains: mdx dystrophic mice; MyoD(-/-) mice that lack expression of the early myogenic regulatory gene MyoD; and a double-mutant mdx:MyoD(-/-) strain lacking expression of both MyoD and dystrophin. We tested the hypothesis that differences in spectra according to genotype and the regeneration phenotype are related specifically to proliferation by committed myogenic precursor cells. 1H-NMR distinguished the three mutant strains: Taurine was highest in mdx muscles, with the phenotype of most effective regeneration; lowest in MyoD(-/-) muscles, with the least effective formation of new muscle in repair, as reported previously; and intermediate in double-mutant muscles, now reported to show an intermediate repair phenotype. The early and late muscle precursors (mpcs) expressing myf5 and myogenin were examined for proliferation. Eighteen percent of mdx myf5-positive mpcs were proliferative, whereas myf5-positive mpcs did not proliferate in regenerating muscles that lacked MyoD expression. By contrast, whereas 30% of myogenin-positive mpcs were proliferative in mdx muscles, almost none were proliferative in MyoD(-/-) muscles, and 12% were proliferative in double-mutant muscles. Therefore, the extent of accumulated structural regeneration, taurine levels, and proliferation of late mpc (expressing myogenin) were congruent across genotypes. Proliferation by early mpc (expressing myf5) was inhibited by the lack of MyoD expression during muscle regeneration. These studies indicate the potential for 1H-NMR monitoring of muscle status in disease, regeneration, and treatment.

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Taurine: Biological Update

Cited by 552 publications

References 3 publications

Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia

Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia

Antioxidant Effect of Taurine Against Lead-Induced Oxidative Stress

Regeneration and myogenic cell proliferation correlate with taurine levels in dystrophin- and MyoD-Deficient muscles

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