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PubMed1990

The interaction between ethanol and cysteine on the central depressant effects of ethanol in mice.

In this study male Swiss-Webster mice were used to examine the effects of cysteine (ICV), a precursor in the biosynthesis of taurine, on ethanol-induced loss of the righting reflex. The interaction of ethanol with gamma-aminobutyric acid (GABA) and isethionic acid, a metabolite of taurine, was also investigated on ethanol-induced central nervous system depression as measured by loss of the righting reflex experiments. Immediately after the animals regained the righting reflex following ethanol injection (IP) mice received an ICV injection of saline, cysteine (1, 15 or 25 mumol/kg), GABA (1, 15 or 25 mumol/kg) or isethionic acid (25 or 50 mumol/kg). Upon ICV administration of cysteine or GABA the mice again lost the righting reflex. This effect occurred immediately and in a dose-dependent manner. The compound, isethionic acid, failed to cause a second loss of the righting reflex following ethanol administration (IP). In the absence of ethanol cysteine or GABA (25 mumol/kg, ICV) did not produce a substantial loss of the righting reflex in mice. In another experiment mice were pretreated (IP) with L-2-oxothiazolide-4-carboxylate (OTC) 2 hr prior to ethanol administration (IP). OTC is a compound which can be converted to cysteine in the body. In the presence of ethanol OTC (15 mmol/kg) caused an enhancement of ethanol-induced central nervous system depression under certain conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Inhibition of rat vascular smooth muscle cell proliferation by taurine and taurine analogues.

The growth of rat aorta vascular smooth muscle cells (VSMCs) was measured in the presence and absence of taurine. Concentrations of taurine as low as 0.3 mM in the culture medium inhibited the proliferation of the cells, as monitored by measuring cell count, and also inhibited the rate of DNA synthesis, as examined by measuring [3H]thymidine incorporation into DNA. However, even at the highest concentration of taurine (30 mM), the doubling time of the VSMCs was only increased by 38%. Protein content of the VSMCs was decreased by 30 mM taurine. [3H]Leucine incorporation into newly synthesized protein was not affected by the highest concentration of taurine tested (30 mM), indicating that taurine did not inhibit protein synthesis but rather decreased total protein content by inhibiting cellular proliferation. The effects of other amino acids such as alanine, glycine, and serine and of various taurine analogues such as beta-alanine, guanidinoethanesulfonic acid (GES), and isethionic acid also were tested at a concentration of 20 mM for their effects on the growth of the VSMCs. Alanine, glycine, and serine had only a minimal effect or no effect on cell count, quantity of protein, and incorporation of [3H]thymidine into DNA. GES, beta-alanine, and isethionic acid had a significant effect on cell count, protein content, and incorporation of [3H]thymidine into DNA. Beta-alanine was the only analogue tested that significantly depressed [3H]leucine incorporation into newly synthesized protein. It is concluded that taurine, GES, and isethionic acid inhibited proliferation of VSMCs but did not alter normal protein synthesis or survivability of VSMCs. In contrast, other amino acids, alanine, glycine and serine, had minimal effects on VSMC proliferation and protein synthesis, whereas beta-alanine appeared to be toxic, inhibiting both VSMC synthesis and de novo protein synthesis.

Amino Acids↗
PubMed2000

Induction of metamorphosis in the sea urchin Holopneustes purpurascens by a metabolite complex from the algal host Delisea pulchra.

Most benthic invertebrates have complex life cycles with planktonic larvae that return to the substratum to settle and metamorphose into a benthic stage. Although naturally produced chemical cues have long been thought to be important for the settlement or metamorphosis of invertebrate larvae, few ecologically relevant chemical cues have been clearly identified. The marine echinoid Holopneustes purpurascens has a complex life cycle, with a planktonic, nonfeeding dispersive larva that metamorphoses into a benthic stage that lives in the canopy of subtidal benthic algae such as the red alga Delisea pulchra and the kelp Ecklonia radiata. Recently recruited juveniles are found primarily on D. pulchra, and we hypothesized that this was in response to a chemical cue produced by this alga. Competent larvae metamorphosed in the presence of D. pulchra, or seawater surrounding this alga, but not in response to the presence of E. radiata or its extracts. A cue for metamorphosis was isolated and characterized from D. pulchra and found to be a water-soluble complex of the sugar floridoside and isethionic acid in a 1:1 molar ratio. The floridoside-isethionic acid complex also triggered settlement in H. purpurascens; however, this response was less specific than metamorphosis and was reversible. Larvae of H. purpurascens also metamorphosed in the presence of several other species of red, but not brown or green, algae from their habitat. Floridoside is found only in red algae, suggesting that the floridoside-isethionic acid complex may be acting as a cue for metamorphosis in other red algae as well as in D. pulchra.

Animals↗
PubMed2000

Cytoprotective effect of taurine against hypochlorous acid toxicity to PC12 cells.

Taurine has been shown to be an effective scavenger of hypochlorous acid (HOCl). The role of HOCl is well established in tissue damage associated with reperfusion injury mediated by neutrophils. The role of HOCl in CNS injury and inflammatory reactions has not been well established. Myeloperoxidase activity is present in the CNS and it has been associated with ischemic injury. The aim of the present study was to determine the cytotoxicity of HOCl in a neuronal cell line (PC12) and the ability of taurine to prevent or reverse neurotoxicity. PC12 cells were grown in 96 well plates at a plating density of approximately 100,000 cells per well. HOCl was made up fresh from NaOCl for each experiment and the concentration verified spectrophotometrically. PC12 cells were exposed to HOCl for 1 hour in phosphate-buffered saline. Taurine was added at the time of HOCl treatment and in some experiments a post-treatment with taurine was performed by adding 1 or 10 mM taurine to the culture media (RPMI 1640). The cells were allowed 24 hours to recover and viability was determined using a tetrazolium-based (MTT) assay. The first series of experiments evaluated the toxicity of HOCl and the efficacy of taurine to protect PC12 cells. HOCl at 50 microM reduced PC12 cell viability by 50% and 150 microM reduced viability to <25% of control levels. Taurine (0.5-20 mM) was tested for cytoprotection against 150 microM HOCl and PC12 cells treated with 0.5 mM taurine exhibited only a 20% reduction in viability compared to untreated controls. Taurine concentrations of 1 mM or higher provided nearly 100% protection against HOCl. A second study was performed comparing taurine to beta-alanine, glutathione and isethionic acid. HOCl (100 microM) reduced viability to 25 +/- 1% of controls and taurine, beta-alanine and glutathione at 1 mM provided nearly complete protection. In contrast, isethionic acid, which lacks an amino group, failed to provide protection. Taurine (1 or 10 mM) added after 50 microM HOCl treatment did not provide any protection and PC12 cell viability was reduced to <39% of controls. In contrast, if taurine (50 microM) was present during the HOCl treatment and 1 mM taurine was added after the treatment, PC12 cell viability was 80 +/- 5% of controls. A combination of 250 microM taurine during the HOCl treatment and 1 mM taurine post-treatment produced 100% protection. These results clearly show that taurine is an efficient scavenger of HOCl and can prevent neuronal damage caused by HOCl. Since myeloperoxidase expression in the CNS is increased by ischemia, one function of taurine released during an ischemic event may be to scavenge HOCl and provide neuroprotection.

Animals↗
PubMed1999

Potentiation of mitochondrial Ca2+ sequestration by taurine.

The effects of taurine (2-aminoethanesulphonic acid) and its analogues, 2-aminoethylarsonic acid, 2-hydroxyethanesulphonic (isethionic) acid, 3-aminopropanesulphonic acid, 2-aminoethylphosphonic acid, and N,N-dimethyltaurine, were studied on the transport of Ca2+ by mitochondria isolated from rat liver. Taurine enhanced Ca2+ uptake in an apparently saturable process, with a Km value of about 2.63 mM. Taurine behaved as an uncompetitive activator of Ca2+ uptake, increasing both the apparent Km and Vmax values of the process. This effect was not modified in the presence of cyclosporin A (CsA). N,N-Dimethyltaurine also stimulated Ca2+ uptake at higher concentrations, but there was no evidence that the process was saturable over the concentration range used (1-10 mM). Aminoethylarsonate was a weak inhibitor of basal Ca2+ uptake, but inhibited that stimulated by taurine in an apparently competitive fashion (Ki = 0.05 mM). The other analogues had no significant effects on this process. Taurine either in the presence or the absence of CsA had no effect on Ca2+ release induced by 200 nM ruthenium red. Thus, the mechanism of taurine-enhanced Ca2+ accumulation appears to involve stimulation of Ca2+ uptake via the uniport system rather than inhibition of Ca2+ release via the ion (Na+/Ca2+ and/or H+/Ca2+) exchangers or by taurine modulating the permeability transition of the mitochondrial inner membrane. Overall, these findings indicate an interaction of taurine with an as yet unidentified mitochondrial site which might regulate the activity of the uniporter. The unique role of taurine in modulating mitochondrial Ca2+ homeostasis might be of particular importance under pathological conditions that are characterised by cell Ca2+ overload, such as ischaemia and oxidative stress.

Animals↗
PubMed2004

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.

Perfusion with high millimolar levels of taurine evoked a long-lasting 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 beta-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 (beta-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.

Animals↗
PubMed1975

Cortical and subcortical projected foci in cats: inhibitory action of taurine.

The effects of local application of taurine and isethionic acid on the propagation of the epileptic activity to the mirror area in cats have been studied. Cortical and amygdaloid acute foci were induced by local administration of conjugated estrogens. Taurine proved to be effective in reducing and sometimes in abolishing the appearance of the epileptic propagated elements in the mirror area. When this agent was applied 30 minutes before the induction of the primary focus, the single spike transmission was reduced or prevented; however, the transmission of a seizure was not blocked. No changes in the transmitted phenomena were observed when isethionic acid was administered with the same technique as that used for taurine. The present study stresses the clear antiepileptic activity of taurine in this experimental model, ruling out the possibility of an unspecific interaction with the epileptogenic agents. Moreover, it is suggested that the deamination of taurine is not important for its antiepileptic action.

Amygdala↗
PubMed2004

NMR 13C-isotopic enrichment experiments to study carbon-partitioning into organic solutes in the red alga Grateloupia doryphora.

The red alga Grateloupia doryphora Montagne (Howe) (Cryptonemiales, Halymeniaceae) was used as a model to investigate the effects of changes in seawater salinity on the intracellular low-molecular-weight organic compounds. Carbon-partitioning into major organic solutes was followed by 13C nuclear magnetic resonance (NMR) spectroscopy on living algae incubated in NaH13CO3-enriched seawater, and by high resolution 1H and 13C NMR experiments performed on 13C-enriched algal extracts. NMR and high performance liquid chromatography (HPLC) analyses both demonstrated that floridoside level was the most affected by changes in salinity: it rose under the hypersaline treatment and decreased under hyposaline one. Moreover, at low salinity, the high labeling of floridoside (45.3% 13C-enrichment for C1) together with its low concentrations both provided evidence of great increase in the de novo biosynthesis and turnover rate. Our experiments also demonstrated a high incorporation of photosynthetic carbon into amino acids, especially glutamate, under hypoosmotic conditions. On the other hand, isethionic acid and N-methyl-methionine sulfoxide were only partly labeled, which indicates they do not directly derive from carbon photoassimilation. In algae exposed to high salinity, elevated concentrations of floridoside coupled to a low labeling (9.4%) were observed. These results suggest that hyperosmotic conditions stimulated floridoside biosynthesis from endogen storage products rather than from carbon assimilation through photosynthesis.

Amino Acids↗
PubMed1983

Sulfate transport by flounder renal tubule brush border: presence of anion exchange.

Transport of sulfate into brush border membrane (BBM) vesicles from renal tubules of southern flounder, Paralichthys lethostigma, was investigated. Imposition of a 21 mM HCO-3 gradient, in greater than out, produced concentrative sulfate uptake (overshoot) fourfold higher than equilibrium. Gradient conditions were necessary to produce this response; no overshoot was produced by the mere presence of HCO-3. Generation of potassium diffusion potentials with KCl gradients and valinomycin or short-circuiting of possible other ionic diffusion potentials had no effect on sulfate uptake. The rate-limiting step in HCO-3:SO2-4 exchange is, therefore, an electroneutral process. Although HCO-3 was the most effective counterion for sulfate, SCN-, Cl-, and S2O2-3 were also capable of promoting concentrative sulfate uptake. Sulfate uptake in the absence of counterion and bicarbonate-dependent sulfate uptake were both shown to be saturable processes. HCO-3-driven sulfate uptake could be inhibited by disulfonic stilbene, HgCl2, probenecid, chlorophenol red, and bromcresol green. Phloridzin, p-aminohippuric acid, 2,4-dinitrophenol, isethionic acid, and citric acid had no significant effect on HCO-3:SO2-4 exchange. The role of this sulfate:anion exchanger in active renal tubule sulfate secretion is discussed.

Adenosine Triphosphatases↗
PubMed1955

On the chemical composition of the axoplasm of squid giant nerve fibers with particular reference to its ion pattern.

Investigations dealing with the determination of the major chemical constituents of the axoplasm of the giant nerve fiber of the squid are described. Particular emphasis has been placed on determining the components involved in acid-base balance. It was found that 72 per cent of the total solids of axoplasm, representing 13.5 per cent of the wet material, are of relatively low molecular weight (dialyzable) and consist mainly of charged ionic or dipolar constituents. Of the 520 micromoles per gm. of total base, 72 per cent are balanced by organic acids: aspartic acid (65 micro equivalents per gm.), glutamic acid (10 micro equivalents), fumaric and succinic acids (15 micro equivalents), a new polycarboxylic acid (35 micro equivalents), and isethionic acid, a biologically novel sulfonic acid (220 micro equivalents). Besides potassium, sodium, small amounts of calcium, and magnesium there is a considerable fraction of organic (nitrogenous) base. Other features of the chemical composition of squid axoplasm include a relatively high concentration of taurine (100 micro equivalents) and an ultraviolet absorbing substance possibly identical with N-methylpicolinic acid. The distribution of the phosphates, especially the concentration of ATP, has been investigated. Specific techniques elaborated in connection with this study have been described and the biochemical implications of the analytical results are discussed.

Acid-Base Equilibrium↗
PubMed1978

Characterization of a carrier-mediated transport system for taurine in the fetal mouse heart in vitro.

Cardiac taurine levels are elevated in hypertension and congestive heart failure. A possible mechanism for this increase in taurine is an alteration of its uptake. We sought to identify and characterize a carrier-mediated transport system for taurine in the mammalian myocardium utilizing the fetal mouse heart in organ culture. Hearts from fetuses of 16-19 days gestational age used in these studies had an endogenous taurine content of 14.1+/-0.5 nmol/mg tissue. The uptake of [(3)H]taurine was linear for up to 8 h. Taurine was accumulated against a concentration gradient as demonstrated by a net increase in taurine concentration when hearts were incubated in 0.5 mM taurine. [(3)H]Taurine uptake was saturable, K(m) = 0.44 mM, temperature dependent, and required sodium. The close structural analogues, hypotaurine and beta-alanine, reduced [(3)H]taurine uptake by 87% when present in 100-fold excess. The alpha-amino acids alanine, alpha-aminoisobutyric acid, glycine, leucine, and threonine did not inhibit uptake. Other taurine analogues tested were guanidinotaurine, guanidinopropionic acid, gamma-aminobutyric acid, 2-aminoethane phosphonic acid, aminomethane sulfonic acid, 3-aminopropane sulfonic acid, N-acetyltaurine, and isethionic acid. We conclude that a carrier-mediated transport system for taurine exists in the fetal mouse heart based on the demonstration of (a) temperature dependence, (b) saturability, and (c) structural selectivity of the uptake process. Transport was demonstrated to be mediated by a beta-amino acid uptake system. In addition, taurine uptake was observed to be sodium dependent, energy dependent, and capable of accumulating taurine against a concentration gradient.

Animals↗
PubMed1975

Metabolism of [35S]taurine in man.

Taurine metabolism in man was defined by an isotope dilution technique during normal taurine intake (five subjects) or increased taurine intake (two subjects). A tracer dose of [35S]taurine was administered intravenously, and the amount and chemical form of radioactivity were determined in blood, urine, bile, and feces. Analysis of plasma specific activity decay curves indicated that taurine metabolism can be described by two exchangeable pools: a small (2 mmoles), rapidly exchanging pool (t1/2 approximately equal to 0.1 hour); and a large (98 mmoles), very slowly exchanging pool (t1/2 approximately equal to 70 hours). A small amount of [35S]isethionic acid was detected in urine, possibly the result of deamination of taurine by tissues; but otherwise no evidence of tissue biotransformation was obtained. Taurine was excreted predominantly (95%) in urine, about 70% as taurine and 25% as sulfate. The sulfate was considered to be formed in the intestine by bacterial degradation of taurine and then absorbed. Supplemental taurine (given orally) was well absorbed, caused a transient increase in plasma taurine levels, was excreted in urine without equilibration with the slowly exchangeable pool, and caused only a modest increase in total body taurine. Thus, taurine resembles other amino acids in having large tissue pools but differs strikingly in being metabolically inert with an extremely slow turnover rate.

Adult↗
PubMed1980

Contralateral circling behaviour induced by intranigral injection of taurine in rats.

A study was made of the effect of unilateral injection of taurine into the substantia nigra on the behaviour of rats. Taurine (10-200 micrograms) induced a dose-dependent contralateral circling behaviour. The maximum intensity of circling after doses of 100-200 micrograms of taurine was reached within 10 min. and the circling lasted for about 4-5 hrs. There was neither ipsilateral circling nor stereotyped behaviour. Intranigral injection of isethionic acid, a metabolite of taurine, induced weak ipsilateral circling of short duration. Pretreatment with bicuculline (3 mg/kg intraperitoneally) or strychnine (0.25 mg/kg intraperitoneally) significantly inhibited the taurine-induced circling. A dose of 1 mg/kg but not of 0.5 mg/kg of haloperidol (subcutaneously) significantly decreased the intensity of the taurine-induced circling. Pretreatment with atropine (10 mg/kg intraperitoneally) had no significant effect on the circling behaviour. Besides the dopaminergic nigrostriatal pathway, the nondopaminergic nigral output pathways also seem to be involved in the taurine-induced circling behaviour. The results show that taurine may play some role in the function of the substantia nigra.

Animals↗