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PubMed2001

Taurine is a weak scavenger of peroxynitrite and does not attenuate sodium nitroprusside toxicity to cells in culture.

Many studies have suggested an antioxidant role for taurine, but few studies have directly measured its free radical scavenging activity. The aim of the present study was to directly determine the action of taurine and taurine analogs to inhibit peroxynitrite-mediated oxidation of dihydrorhodamine 123 (DHR) to rhodamine. Taurine was also tested to determine if it could attenuate the toxicity of sodium nitroprusside (SNP) to neuronal cultures. Taurine at concentrations above 30 mM had a modest ability to inhibit peroxynitrite formation derived from SIN-1. Hypotaurine could inhibit peroxynitrite formation from both SIN-1 (decrease 75%) and SNP (decrease 50%) at 10 mM. Other taurine analogs (homotaurine, beta-alanine & isethionic acid) slightly potentiated DHR oxidation by SIN-1. Short-term (1-hour) treatment of PC12 cultures with either SNP (1-2mM) or taurine (20-40 mM) appeared to induce cellular proliferation. In contrast, 24-hour treatment with SNP (1 mM) induced cell death. Combination treatments with taurine and SNP appeared to interact in an additive fashion for both cell proliferation and neurotoxic actions. It appears unlikely that taurine is a major endogenous scavenger of peroxynitrite.

Animals↗
PubMed1995

Taurine allosterically inhibits binding of [35S]-t-butylbicyclophosphorothionate (TBPS) to rat brain synaptic membranes.

The modulatory effects of taurine on [35S]-t-butylbicyclophosphorothionate (TBPS) binding to rat brain synaptic membranes were evaluated and compared with that of GABA. Taurine allosterically inhibited TBPS binding by interacting with a bicuculline-sensitive site, similar to GABA. Taurine was as effective as GABA but less potent. The potency of taurine inhibition of TBPS binding varied among brain regions with cerebellum > olfactory bulb > cortex, similar to that of GABA. Inhibition of TBPS binding to cortical membranes measured under nonequilibrium conditions yielded a dynamic biphasic inhibition curve that was similarly shaped for GABA and taurine. The effect of taurine on TBPS binding was pharmacologically specific in that beta-alanine and guanadinoethanesulfonate were as effective as taurine, while hypotaurine and alpha-aminoethylhydrogen sulfate were only partially effective at high concentrations, and isethionic acid was without effect. Taurine, similar to GABA, enhanced the effects of pentobarbital on TBPS binding when present at concentrations that were otherwise ineffective on their own. The results of these studies support the notion that taurine interacts with the GABA recognition site of the GABAA receptor complex.

Allosteric Regulation↗
PubMed1985

Effects of taurine on calcium ion uptake and protein phosphorylation in rat retinal membrane preparations.

The effects of taurine on ATP-dependent calcium ion uptake and protein phosphorylation of rat retinal membrane preparations were investigated. Taurine (20 mM) stimulates ATP-dependent calcium ion uptake by twofold in crude retinal homogenates. In contrast, it inhibits the phosphorylation of specific membrane proteins as shown by acrylamide gel electrophoresis and autoradiography. The close structural analogue of taurine, 2-aminoethylhydrogen sulfate, demonstrates similar effects in both systems, i.e., stimulation of ATP-dependent calcium ion uptake and inhibition of protein phosphorylation, whereas isethionic acid and guanidinoethanesulfonate have no effect on either system. A P1 subcellular fraction of the retinal membrane preparation that contains photoreceptor cell synaptosomes has a higher specific activity for the uptake of calcium ions. Phosphorylation of specific proteins in the P1 fraction is also inhibited by the addition of 20 mM taurine. Taurine has no effect on retinal ATPase activities or on phosphatase activity, thus suggesting that it directly affects a kinase system.

Adenosine Triphosphate↗
PubMed1988

ATP-dependent glutamate uptake into synaptic vesicles from cerebellar mutant mice.

The ATP-dependent glutamate uptake system in synaptic vesicles prepared from mouse cerebellum was characterized, and the levels of glutamate uptake were investigated in the cerebellar mutant mice, staggerer and weaver, whose main defect is the loss of cerebellar granule cells, and the nervous mutant, whose main defect is the loss of Purkinje cells. The ATP-dependent glutamate uptake is stimulated by low concentrations of chloride, is insensitive to aspartate, and is inhibited by agents known to dissipate the electrochemical proton gradient. These properties are similar to those of the glutamate uptake system observed in the highly purified synaptic vesicles prepared from bovine cortex. The ATP-dependent glutamate uptake system is reduced by 68% in the staggerer and 57-67% in the weaver mutant; these reductions parallel the substantial loss of granule cells in those mutants. In contrast, the cerebellar levels of glutamate uptake are not altered significantly in the nervous mutant, which has lost Purkinje cells, but not granule cells. In view of evidence that granule cells are glutamatergic neurons and Purkinje cells are GABAergic neurons, these observations support the notion that the ATP-dependent glutamate uptake system is present in synaptic vesicles of glutamatergic neurons.

Adenosine Triphosphate↗
PubMed1976

Taurine transport rates between plasma and tissues in adult and 7-day-old mice.

Transport rates for taurine from plasma to liver, kidney, heart, spleen and femoral muscle were evaluated in adult and 7-day-old mice in vivo. The mice were injected with [35S]taurine and the specific radioactivity of taurine was determined in the above tissues at varying intervals from 10 min up to 48 hr after the injection. A multicompartment model was fitted to the data and the transport rates with their confidence limits were estimated using a digital computer. The tissue-plasma exchange rate was generally faster in adult mice than in 7-day-old mice. The transport rates between the plasma and the brain or muscle were low, while taurine penetrated into the liver and kidneys very rapidly. There was no distinct correlation between the calculated transport rates and the tissue taurine concentrations. The metabolic breakdown of taurine in the tissues was slow, since only negligible amounts of radioactivity were recovered in the metabolites of taurine, isethionic acid and inorganic sulphate. It seems unlikely that either the magnitudes of the transport rates between the plasma and the tissues or taurine breakdown rates in situ act as the primary factor determining the taurine levels in tissues.

Animals↗
PubMed1982

Characteristics of the release of the surface coat protein from bloodstream forms of Trypanosoma brucei.

Bloodstream forms of the African trypanosomes undergo antigenic variation in their mammalian host. This process involves removal of the existing variant coat protein and its replacement with another. The mechanism by which the surface coat protein is released to the external supporting medium has been shown to depend in vitro specifically on the presence of calcium ions together with the calcium ionophore. A-23187, and to be inhibited by Zn2+. Release of the surface coat protein was not stimulated by conditions designed to alter the plasma membrane potential or the major ionic gradients across that membrane. Release could be stimulated by inhibiting the energy metabolism of these glycolysing cells with 2-deoxyglucose, which probably prevents the energy-dependent mechanisms that normally keep the cytoplasmic Ca2+ concentration low. These results and the finding that the release process was strongly temperature dependent suggested the possible mediation of some as yet undefined enzymatic reaction.

Animals↗
PubMed1981

The asymmetric transmembrane distribution of phosphatidylethanolamine, phosphatidylserine, and fatty acids of the bovine retinal rod outer segment disk membrane.

The transmembrane distribution of the major aminophospholipids in the bovine retinal rod outer segment disk membrane, phosphatidylethanolamine and phosphatidylserine, was determined using a novel pair of permeable and impermeable covalent modification reagents. The values for the percentages of phosphatidylethanolamine and phosphatidylserine in the outer monolayer were calculated from a simple expression which takes into account the leakage of impermeable reagent into the disk lumen as monitored by the extent of labeling of lysine entrapped in the lumen. We infer from our results that at least 73 to 87% of the disk phosphatidylethanolamine and 77 to 88% of the disk phosphatidylserine are in the outer disk membrane monolayer. The fatty acid composition of the inner aminophospholipids is slightly more saturated than the outer aminophospholipids. Calculations using the lateral surface areas occupied by the disk membrane lipids suggest that 65 to 100% of the disk phosphatidylcholine is on the inner membrane surface. Since the disk phosphatidylcholine is also somewhat more saturated than the phosphatidylethanolamine and phosphatidylserine of the outer monolayer, the total inner membrane monolayer fatty acid composition is more saturated than that of the outer monolayer fatty acid composition.

Animals↗
PubMed1985

Characterization of glutamate uptake into synaptic vesicles.

Recent evidence indicates that L-glutamate is taken up into synaptic vesicles in an ATP-dependent manner, supporting the notion that synaptic vesicles may be involved in glutamate synaptic transmission. In this study, we further characterized the ATP-dependent vesicular uptake of glutamate. Evidence is provided that a Mg-ATPase, not Ca-ATPase, is responsible for the ATP hydrolysis coupled to the glutamate uptake. The ATP-dependent glutamate uptake was inhibited by agents known to dissipate the electrochemical proton gradient across the membrane of chromaffin granules. Hence, it is suggested that the vesicular uptake of glutamate is driven by electrochemical proton gradients generated by the Mg-ATPase. Of particular interest is the finding that the ATP-dependent glutamate uptake is markedly stimulated by chloride over a physiologically relevant, millimolar concentration range, suggesting an important role of intranerve terminal chloride in the accumulation of glutamate in synaptic vesicles. The vesicular glutamate translocator is highly specific for L-glutamate, and failed to interact with aspartate, its related agents, and most of the glutamate analogs tested. It is proposed that this vesicular translocator plays a crucial role in determining the fate of glutamate as a neurotransmitter.

Adenosine Triphosphate↗
PubMed1986

Localisation of the hydrophilic C terminal part of the ATP synthase subunit 8 of Saccharomyces cerevisiae.

The hydrophobic subunit 8 of the yeast ATP synthase was modified using the non-penetrating amino reactive specific reagent: isethionylacetimidate. The polypeptide was modified when using the isolated ATP synthase and sodium bromide-treated submitochondrial particles. It is shown that the only lysine of the protein was modified by the reagent. It is concluded that the hydrophilic C terminal part of the protein containing lysine 47 is located on the inner side of the inner mitochondrial membrane.

Amino Acid Sequence↗
PubMed1989

Evidence that alteration of charge modifies proximal tubular shunt pathway permselectivity.

Experiments were performed to test the hypothesis that membrane charge is an important determinant of paracellular pathway ion permselectivity in the proximal tubule. Net negative charge in or around the paracellular pathway should favor cation permeability; net positive charge should favor anion permeability. Therefore compounds such as amiloride and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), capable of changing net membrane charge, should predictably change the diffusive permselectivity of the paracellular pathway to anions and cations. In the first group of experiments amiloride, a compound capable of increasing net positive membrane charge, inhibited cation and enhanced anion diffusive permeability. In a second group of experiments, SITS, a compound capable of increasing net negative membrane charge, inhibited anion and enhanced cation diffusive permeability. The effects of amiloride and SITS were symmetrical; the lumen-to-bath and the bath-to-lumen diffusion potentials were not significantly different in magnitude. In addition these effects were completely and rapidly reversible. Our results suggest that amiloride increases net positive charge, and SITS increases net negative charge within the paracellular pathway. The most likely site for the actions of SITS and amiloride is the tight junction because the effects of the inhibitors were symmetrical. Both compounds act at low concentrations and reversibly such that removal of the inhibitor rapidly reverses its effects. We propose, on the basis of the ease with which these alterations in charge and thus paracellular pathway permselectivity occurred, that the permselectivity of this pathway may not be fixed and constant for any given proximal tubular segment. In fact, permselectivity may vary and thus serve as an important physiological control mechanism for proximal tubular solute and water reabsorption.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1993

Ionic mechanisms underlying the depolarizing and hyperpolarizing afterpotentials of single spike in guinea-pig cingulate cortical neurons.

Intracellular recordings and hybrid single-microelectrode voltage-clamp techniques were used to study the ionic mechanisms underlying the afterdepolarization and the subsequent slow afterhyperpolarization that followed a single action potential in layers V/VI neurons of the guinea-pig anterior cingulate cortex in in vitro slices. Both the afterdepolarization and afterhyperpolarization were markedly suppressed in size by addition of Co2+ or Cd2+, reduction in extracellular Ca2+, and intracellular EGTA injection. On the other hand, elevation of extracellular Ca2+ concentration augmented the amplitudes of the afterpotentials. The afterdepolarization amplitude was selectively depressed by the stilbene derivatives, 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonate, disodium 3H2O, and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid, disodium salt. Reduction in external Cl- and intracellular Cl- injection enhanced the afterdepolarization amplitude without affecting the afterhyperpolarization. The null potentials for the afterdepolarizations recorded with K acetate- and Cs acetate-electrodes were -68 and -63 mV, respectively. The slope of the null potential obtained with K acetate electrodes or Cs acetate electrodes was 49 and 53 mV, respectively, per log unit of the external Cl- concentration. Reduction in external K+ markedly depressed the afterdepolarization and augmented the afterhyperpolarization in size, whereas rise in external K+ markedly augmented the afterdepolarization and depressed the afterhyperpolarization. The null potential for the afterhyperpolarization recorded with K acetate electrodes was -94 mV. The slope of the null potential was 57 mV per log unit of the external K+ concentration. Reduction in extracellular Na+ concentration slightly depressed both the amplitudes of the afterdepolarization and afterhyperpolarization. A hybrid voltage-clamp analysis revealed a slow decaying inward current and a subsequent outward current that followed an action potential. Both the amplitudes of the inward current corresponding to afterdepolarization and the outward current corresponding to afterhyperpolarization were suppressed by addition of Co2+. Reduction in extracellular Cl- concentration augmented the inward current amplitude without significantly affecting the outward current. These results indicate that the afterdepolarization is mainly due to an increase in a Ca(2+)-activated Cl- conductance, while the afterhyperpolarization is mainly generated by an activation of Ca(2+)-mediated K+ conductance.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMedDate not supplied

Taurine, analogues and ethanol elicited responses.

The effect of taurine, of some of its precursors and major metabolic products on spontaneous locomotor activity were studied in mice. The effect of taurine and some analogues on certain ethanol-mediated responses were observed. Administration of taurine, 50 mg/kg, IP, did not significantly alter motility in experimental animals compared to controls. Behavioral depression was evident subsequent to injection of cysteine hydrochloride or taurocholic acid (50 mg/kg). Administration of taurocholic acid, 50 mg/kg, IP, 30 min prior to a narcotic dose of ethanol, 5 g/kg, IP, reduced the time required for the onset of ethanol-narcosis. Pretreatment with cysteic acid, 50 mg/kg, IP, prolonged ethanol-produced narcosis. Treatment with cysteic acid 30 min prior to ethanol, 2.5 g/kg, IP, was found to decrease whole blood ethanol concentration as compared to the respective controls without a concomitant changes in brain ethanol levels. Administration of taurocholic acid, 100 mg/kg, IP, decreased the intake of an ethanol solution in rats preferring 5% ethanol solution over water as the drinking fluid of choice. None of the compounds tested altered endogenous specific activity of mouse liver alcohol dehydrogenase when given once daily (50 mg/kg, IP) for 10 consecutive days. The results suggest that both taurocholic acid and cysteic acid exert additive action to some ethanol-elicited responses studied.

Alcohol Drinking↗
PubMed1983

Characterization of a chloride conductance activated by hyperpolarization in Aplysia neurones.

A voltage-clamp study was made of some properties of the non-synaptic hyperpolarization-activated Cl- conductance recently described in Aplysia neurones loaded with Cl- ions (Chesnoy-Marchais, 1982). The experiments were performed on an identified family of neurones, which present cholinergic responses allowing an easy measurement of the equilibrium potentials of Cl- (ECl) and K+ ions (EK). The Cl- selectivity of the hyperpolarization-activated conductance was deduced from four observations: (1) the extrapolated reversal potential of the hyperpolarization-activated current, Er, was close to the reversal potential of the cholinergic Cl- response, which is the equilibrium potential for Cl- ions, ECl. (2) Modifications of the intracellular or extracellular Cl- concentration induced changes of the reversal potential Er. (3) A prolonged and intense activation of the current lowered the intracellular Cl- concentration. (4) The current persisted after complete substitution of intracellular and extracellular cations by CS+ ions, as well as after replacement of extracellular Na+ ions by Tris. The steady-state Cl- conductance (gss) increases steeply with hyperpolarization. The kinetics of activation and deactivation are exponential and are characterized by the same voltage-dependent time constant (tau), of the order of a few seconds or fractions of seconds. The curves gss(V) and tau (V) can both be fitted by a two-state model in which the rate constants are exponential functions of the membrane potential (e-fold change for 12-16 mV). The Cl- current is much more affected by changes of the intracellular Cl- concentration than predicted simply from the change in Cl- driving force. Both the conductance and the time constant of activation are strongly modified. Modifications of the extracellular Cl- concentration do not always alter the amplitude of the hyperpolarization-activated Cl- current, but systematically affect its kinetics. The hyperpolarization-activated current is abolished after prolonged exposure of the cell to an artificial sea water where NO3- ions replace Cl- ions, as well as after intracellular injections of NO3- ions. Increasing the external pH shifts the gss(V) and tau (V) curves to the left. Lowering the external pH has reverse but less pronounced effects. In cells which were not loaded with Cl- ions and did not present the hyperpolarization-activated Cl- current, this current could be detected if the hyperpolarizing jump was preceded by short depolarizing pulses. In cells which were loaded with Cl- ions, the Cl- current became larger after a short depolarizing pulse. In the presence of extracellular Co2+ ions, depolarizing pulses no longer increased the Cl- current.(ABSTRACT TRUNCATED AT 400 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1998

GABA-receptor-independent dorsal root afferents depolarization in the neonatal rat spinal cord.

Dorsal root afferent depolarization and antidromic firing were studied in isolated spinal cords of neonatal rats. Spontaneous firing accompanied by occasional bursts could be recorded from most dorsal roots in the majority of the cords. The afferent bursts were enhanced after elevation of the extracellular potassium concentration ([K+]e) by 1-2 mM. More substantial afferent bursts were produced when the cords were isolated with intact brain stems. Rhythmic afferent bursts could be recorded from dorsal roots in some of the cords during motor rhythm induced by bath-applied serotonin and N-methyl--aspartate (NMDA). Bilaterally synchronous afferent bursts were produced in pairs of dorsal roots after replacing the NaCl in the perfusate with sodium-2-hydroxyethansulfonate or after application of the gamma-aminobutyric acid-A (GABAA) receptor antagonist bicuculline with or without serotonin (5-HT) and NMDA. Antidromic afferent bursts also could be elicited under these conditions by stimulation of adjacent dorsal roots, ventrolateral funiculus axons, or ventral white commissural (VWC) fibers. The antidromic bursts were superimposed on prolonged dorsal root potentials (DRPs) and accompanied by a prolonged increase in intraspinal afferent excitability. Surgical manipulations of the cord revealed that afferent firing in the presence of bicuculline persisted in the hemicords after hemisection and still was observed after removal of their ventral horns. Cutting the VWC throughout its length did not perturb the bilateral synchronicity of the discharge. These findings suggest that the activity of dorsal horn neurons is sufficient to produce the discharge and that the bilateral synchronicity can be maintained by cross connectivity that is relayed from side to side dorsal to the VWC. Antagonists of GABAB, 5-HT2/5-HT1C, or glutamate metabotropic group II and III receptors could not abolish afferent depolarization in the presence of bicuculline. Depolarization comparable in amplitude to DRPs, could be produced in tetrodotoxin-treated cords by elevation of [K+]e to the levels reported to develop in the neonatal rat spinal cord in response to dorsal root stimulation. A mechanism involving potassium transients produced by neuronal activity therefore is suggested to be the major cause of the GABA-independent afferent depolarization reported in our study. Possible implications of potassium transients in the developing and the adult mammalian spinal cord are discussed.

Action Potentials↗