Hypotaurine oxidation by mouse liver tissue.
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Animals↗
Biomedical subjects
P Kontro
Publications and source records attributed to P Kontro.
Synthesis and anticonvulsant properties of some 2-aminoethanesulfonic acid (taurine) derivatives.
A series of 2-acylaminoethanesulfonamides were synthesized by treating the corresponding sulfonyl chlorides with ammonia, a primary, or a secondary amine. A few compounds displayed marked anticonvulsant activity in mice when tested for their potency in the maximal electroshock seizure test. The piperidino, benzamido, phthalimido, and phenylsuccinylimido derivatives were active, whereas the succinylimido, saccharinylimido, and norbornenedicarboxylimido compounds showed no activity. The interference with the sodium-independent taurine binding to mouse brain synaptic membranes was assessed to elucidate the possible mode of anticonvulsant action.
Animals↗
Modulation of noradrenaline uptake and release by taurine in rat cerebral slices.
The effects of taurine on the uptake and release of noradrenaline were studied in forebrain slices from control rats and from rats treated with a taurine-free diet supplemented with 2-guanidinoethanesulphonate. Exogenous taurine slightly increased noradrenaline uptake in slices from untreated rats. There were no significant effects by exogenous taurine on spontaneous efflux of noradrenaline. The potassium-stimulated noradrenaline release was enhanced by taurine from frontal cortical slices and suppressed from occipital slices but only in the diet group, in which the endogenous brain taurine concentration had been lowered to one-half of the control concentration. It is suggested that taurine may act via presynaptic alpha-adrenoceptors and/or modify the availability of calcium for the stimulus-secretion coupling process.
Animals↗
Free amino acids and the uptake and binding of taurine in the central nervous system of rats treated with guanidinoethanesulphonate.
The content of free amino acids in the central nervous system, the uptake of taurine by slices and synaptosomes and taurine binding to synaptic membranes have been studied on adult male Wistar rats after a prolonged administration of 2-guanidinoethanesulphonate with or without a taurine-free diet. The 2-guanidinoethanesulphonate administration both alone and together with a taurine-free diet considerably reduced taurine levels in all regions studied, viz. cerebrum, cerebellum, brain stem and spinal cord, but the contents of methionine and gamma-aminobutyric acid were increased. On the normal diet the maximal taurine loss occurred after a 3-week 2-guanidinoethanesulphonate administration, when also the 2-guanidinoethanesulphonate accumulation in the cerebrum was largest. On the taurine-free diet the taurine levels were still low after the 4-week 2-guanidinoethanesulphonate administration when the taurine content in cerebral synaptosomes was also reduced to almost one half. 2-Guanidinoethanesulphonate treatment modified the uptake and binding processes of taurine in the synaptosomal preparations. The maximal high-affinity taurine uptake was reduced, whereas the affinity of the specific sodium-independent binding sites for taurine increased. The results suggest that the neuromodulator properties of taurine could be affected by the reduced taurine levels and/or by the accumulated 2-guanidinoethanesulphonate.
Amino Acids↗
Taurine and hypotaurine transport by a single system in cultured neuroblastoma cells.
The kinetics of mutual inhibition of taurine and hypotaurine uptake were studied using neuroblastoma C1300 cells as neuronal model. Hypotaurine and GABA inhibited taurine uptake competitively, increasing the apparent Km. High-affinity uptake of hypotaurine was completely abolished and the low-affinity component competitively inhibited by taurine. GABA affected noncompetitively low-affinity hypotaurine uptake, whereas the effect on high-affinity uptake was competitive, with an increase in the apparent Km. All structural analogues tested inhibited taurine and hypotaurine uptakes similarly. The most potent inhibitors were beta-alanine and 2-guanidinoethanesulphonic acid. The mutual inhibition and similar specificity profiles of taurine and hypotaurine uptakes showed that these amino acids employ a single transport system in neuroblastoma cells. Competitive inhibition by GABA of the high-affinity uptake of taurine and hypotaurine further suggests that also GABA uses the same carrier system.
Biological Transport↗
GABA, taurine and hypotaurine in developing mouse brain.
The cerebral concentrations and synaptosomal uptake of taurine and hypotaurine, two putative neuromodulators, were compared with those of GABA, an established neurotransmitter, in developing mice starting from the birth until 3 months of age. The taurine and hypotaurine contents of blood serum and the sodium-independent binding of GABA and taurine to synaptic membranes were also monitored. In the brain the maximum concentration level was reached for taurine at one week, for hypotaurine at 3 weeks, and for GABA at 4 weeks of age. In the serum the hypotaurine content was maximal in the youngest mice (1-week-old) and the taurine concentration during the three first weeks of life. The uptakes of GABA, taurine and hypotaurine were also high during the first three weeks of age, subsequently declining to a constant level. GABA binding to brain membranes was highest at 2 weeks of age. Taurine binding was also higher in the immature than in the adult brain. These developmental alterations suggest that GABA, taurine and hypotaurine are already functionally active in the brain in early postnatal life.
Amino Acids↗
Effects of prolonged guanidinoethanesulphonate administration on taurine and other amino acids in rat tissues.
In order to deplete tissue taurine, 2-guanidinoethanesulphonate, a structural analogue of taurine was administered in drinking water with taurine-free diet to adult rats for four weeks. As a consequence the taurine concentrations in the blood serum, liver, kidney, spleen, intestine, lung, heart, muscle and cerebellum fell by nearly one half. Threonine, serine, glycine, alanine, methionine, tyrosine, lysine and histidine concentrations increased in blood plasma. Similar changes were also discernible in the heart and muscle. In the kidney and the lung the concentrations of several other amino acids fell as well, though increments occurred in the threonine content in the kidney and in threonine, serine and methionine contents in the lung. Taurine was practically the only amino acid the level of which fell in the liver, spleen, intestine and cerebellum. These findings indicate that 2-guanidinoethanesulphonate combined with taurine-free diet effectively lowers tissue taurine levels, but its action is not specific to taurine. It may be used as a tool to elucidate the physiological functions of taurine in the body.
Amino Acids↗
Anticonvulsant activity of some 2-aminoethanesulphonic acid (taurine) derivatives.
A number of aliphatic 2-aminoethanesulphonic acid (taurine) derivatives were tested for their anticonvulsant activity in maximal electroshock seizure and pentylenetetrazole seizure threshold tests in mice. Certain piperidino, benzamido, phthalimido and phenylsuccinylimido derivatives were effective. Phthalimidoethanesulphon-N-methylamide, which inhibited the binding of both taurine and GABA to isolated synaptic membranes, appeared the best anticonvulsant among the derivatives tested.
Animals↗
Taurine, hypotaurine, and GABA uptake by cultured neuroblastoma cells.
Uptake of [3H]taurine, [35S]hypotaurine, and [3H] gamma-aminobutyric acid (GABA) was studied in neuroblastoma C1300 cells in Krebs-Ringer-Hepes-glucose medium (pH 7.4). The uptakes consisted of nonsaturable penetration (taurine and hypotaurine) and two saturable transport components: high affinity for taurine, hypotaurine, and GABA and low affinity for hypotaurine and GABA. The affinity of the high-affinity uptake was highest for hypotaurine but the transport capacity was greatest for taurine. GABA uptake was almost abolished by taurine and hypotaurine. Hypotaurine also strongly inhibited taurine uptake, whereas GABA had only a moderate inhibitory effect on taurine and hypotaurine uptakes. The mutual inhibition suggests that these amino acids use the same transport sites when entering the cells.
Absorption↗
Sodium-independent taurine binding to brain synaptic membranes.
Saturable sodium-independent taurine binding to mouse and rat brain synaptic membranes was exposed after two freezing-thawing cycles combined with Triton X-100 treatments. The amount of saturable taurine binding was fairly low but was enhanced after depletion of brain taurine. Saturable taurine binding was displaceable by some convulsants and anticonvulsants but is specificity still remains to be established.
Animals↗
Mutual interactions in the transport of taurine, hypotaurine, and GABA in brain slices.
The mutual interactions and the effects of GABA on the saturable transport components of taurine and hypotaurine were investigated with mouse brain slices. The low-affinity taurine transport was competitively inhibited by both hypotaurine and GABA. Hypotaurine did not alter the kinetic parameters of high-affinity taurine uptake, whereas there occurred some stimulation with GABA, possibly by heteroexchange. Taurine had no significant effects on high-affinity hypotaurine uptake, whereas the low-affinity component was reduced by both taurine and GABA, GABA strongly interfered with the high-affinity hypotaurine uptake, being the preferred substrate in simultaneous uptake experiments. The results confirm that taurine, hypotaurine, and GABA are transported into brain slices by only one two-component system with affinities highest for GABA and lowest for taurine.
Animals↗
beta-Alanine uptake by mouse brain slices.
beta-[3H]Alanine uptake by mouse brain slices was studied in Krebs-Ringer-HEPES-glucose medium (pH 7.4) under O2. The uptake was temperature-sensitive and consisted of two saturable transport components, high- and low-affinity, with kinetic parameters comparable to those of amino acid neurotransmitter candidates. beta-Alanine uptake was strictly sodium-dependent and also inhibited by the omission of potassium and presence of ouabain, suggesting that the transport is mainly fuelled by cation gradients. Sodium ions showed positive cooperative effects in beta-alanine uptake, indicating the association of at least two sodium ions in the transfer of one molecule of beta-alanine. The uptake was strongly inhibited by gamma-aminobutyrate and hypotaurine, the high-affinity uptake component completely disappearing in the presence of hypotaurine. Taurine had no measurable effect. The results suggest that the high-affinity transports of beta-alanine and hypotaurine may be mediated by the same system.
Alanine↗
Hypotaurine transport in mouse brain synaptosomal preparations.
The transport of hypotaurine, the precursor of the probable neuromodulator taurine, was investigated using mouse brain synaptosomal preparations. Hypotaurine uptake was concentrative, energy- and sodium-dependent and strongly inhibited by GABA, L-DABA (L-2,4-diaminobutyric acid) and beta-alanine, suggesting interactions with GABA uptake systems. The uptake consisted of only one saturable transport component both in adult and in 6-day-old brain, being more efficient in the latter.
Adult↗
Efflux of taurine from bovine cerebral cortex synaptosomes: homo- and hetero-trans-stimulation.
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Aminobutyrates↗
Free amino acids in epilepsy: possible role of taurine.
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Amino Acids↗
Taurine and synaptic transmission.
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Animals↗
Binding of taurine to brain synaptic membranes.
An account is given of our endeavours to demonstrate sodium-independent and -dependent taurine binding to brain synaptic membranes. The total and specific sodium-dependent binding and the total sodium-independent binding were fairly easily amenable to characterization, but the disclosure of specific sodium-independent binding succeeded only after repeated freezing and thawing, thorough buffer washes and two Triton X-100 treatments of the membranes. The sodium-independent binding capacity for taurine was rather small and only one type of relatively low-affinity binding site was revealed.
Animals↗
Novel anticonvulsant taurine derivatives.
A number of novel taurine derivatives were tested for their anticonvulsant activity in maximal electroshock seizure and pentetrazole seizure threshold tests in mice. Certain piperidino, benzamido, phthalimido, and phenylsuccinylimido derivatives of taurinamide were effective, the phthalimido derivatives appearing pharmacologically most promising. Possible interferences with the intracellular release, uptake, and membrane binding of taurine and GABA were assessed in an attempt to elucidate the mode of action of the active compounds. Since the uptake and release processes of taurine and GABA were only slightly affected, but the sodium-independent binding of GABA and/or taurine to synaptic membranes strongly inhibited, the test compounds may preferentially act as taurine or GABA receptor agonists.
Animals↗