共查询到20条相似文献,搜索用时 15 毫秒
1.
Summary. Taurine transport in human intestinal epithelial Caco-2 cells was down-regulated by culturing the cells in taurine-containing
media and was up-regulated in a taurine-free medium. This adaptive regulation was associated with changes in both the Vmax
and Km values of taurine transport. A change in the mRNA level of the taurine transporter (TAUT) in this regulation was also
observed. The presence of such a regulatory mechanism for maintaining the intracellular taurine content at a certain level
suggests that taurine plays an important role in the intestinal cell functions. The intracellular taurine content was increased
when Caco-2 cells were exposed to a hypertonic stress. TAUT was up-regulated via the increased expression of TAUT mRNA in
the hypertonic cells, suggesting that taurine serves as an osmolyte and protects the cells from osmotic stress. Similar up-regulation
of TAUT was observed in the small intestine of water-deprived rats.
Received January 25, 2000/Accepted January 31, 2000 相似文献
2.
Taurine and neural cell damage 总被引:22,自引:2,他引:20
Summary. The inhibitory amino acid taurine is an osmoregulator and neuromodulator, also exerting neuroprotective actions in neural
tissue. We review now the involvement of taurine in neuron-damaging conditions, including hypoxia, hypoglycemia, ischemia,
oxidative stress, and the presence of free radicals, metabolic poisons and an excess of ammonia. The brain concentration of
taurine is increased in several models of ischemic injury in vivo. Cell-damaging conditions which perturb the oxidative metabolism
needed for active transport across cell membranes generally reduce taurine uptake in vitro, immature brain tissue being more
tolerant to the lack of oxygen. In ischemia nonsaturable diffusion increases considerably. Both basal and K+-stimulated release of taurine in the hippocampus in vitro is markedly enhanced under cell-damaging conditions, ischemia,
free radicals and metabolic poisons being the most potent. Hypoxia, hypoglycemia, ischemia, free radicals and oxidative stress
also increase the initial basal release of taurine in cerebellar granule neurons, while the release is only moderately enhanced
in hypoxia and ischemia in cerebral cortical astrocytes. The taurine release induced by ischemia is for the most part Ca2+-independent, a Ca2+-dependent mechanism being discernible only in hippocampal slices from developing mice. Moreover, a considerable portion of
hippocampal taurine release in ischemia is mediated by the reversal of Na+-dependent transporters. The enhanced release in adults may comprise a swelling-induced component through Cl− channels, which is not discernible in developing mice. Excitotoxic concentrations of glutamate also potentiate taurine release
in mouse hippocampal slices. The ability of ionotropic glutamate receptor agonists to evoke taurine release varies under different
cell-damaging conditions, the N-methyl-D-aspartate-evoked release being clearly receptor-mediated in ischemia. Neurotoxic
ammonia has been shown to provoke taurine release from different brain preparations, indicating that the ammonia-induced release
may modify neuronal excitability in hyperammonic conditions. Taurine released simultaneously with an excess of excitatory
amino acids in the hippocampus under ischemic and other neuron-damaging conditions may constitute an important protective
mechanism against excitotoxicity, counteracting the harmful effects which lead to neuronal death. The release of taurine may
prevent excitation from reaching neurotoxic levels.
Received January 25, 2000/Accepted January 31, 2000 相似文献
3.
Summary. Taurine and glutamate were monitored by microdialysis technique during various cerebral insults: a. Application of K+ triggered a cortical spreading depression (CSD). Taurine and glutamate increased concomitantly but recovery of glutamate
was faster than that of taurine. b. Application of NMDA induced also CSD but only taurine increased. c. Induction of an infarct
triggered repetitive CSDs. Taurine increased rapidly whereas glutamate rose slowly starting with some delay. d. After induction
of ischemia, taurine and glutamate increased after onset of depolarisation. The increase of glutamate occurred late after
a small, transient increase in parallel with the depolarisation. These data suggest a close functional relationship between
the changes of both amino acids. Therefore, they should be monitored together especially in clinical settings: during excitation,
only taurine will increase; during overexcitation, taurine will also increase but to a higher maximum followed by a moderate
rise of glutamate; after energy failure, taurine will accumulate to its highest level followed by a continuous rise of glutamate.
Received January 25, 2000/Accepted January 31, 2000 相似文献
4.
Summary. Calcium ion (Ca2+) uptake was measured in rod outer segments (ROS) isolated from rat retina in the presence of varying concentrations of CaCl2 in the incubation buffer (1.0–2.5 mM). It is known that taurine increases Ca2+ uptake in rat ROS in the presence of ATP and at low concentrations of CaCl2 (Lombardini, 1985a); taurine produces no significant effects when CaCl2 concentrations are increased to 1.0 and 2.5 mM. With the removal of both taurine and ATP, Ca2+ uptake in rat ROS increased significantly in the presence of 2.5 mM CaCl2. Taurine treatment in the absence of ATP was effective in decreasing Ca2+ uptake at the higher levels of CaCl2 (2.0 and 2.5 mM). Similar effects were observed with ATP treatment. The data suggest that taurine and ATP, alone or in combination,
limit the capacity of the rat ROS to take up Ca2+ to the extent that a stable uptake level is achieved under conditions of increasing extracellular Ca2+, indicating a protective role for both agents against calcium toxicity.
Received January 25, 2000/Accepted January 31, 2000 相似文献
5.
Interaction between the actions of taurine and angiotensin II 总被引:1,自引:0,他引:1
Summary. The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion
of taurine has been linked to developmental defects, retinal damage, immundeficiency, impaired cellular growth and the development
of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy
promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that
responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might
underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through
its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation
of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in
humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses
the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin
II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many
of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling.
Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably
very important.
Received November 10, 1998, Accepted May 19, 1999 相似文献
6.
Marchesi C Dall'Asta V Rotoli BM Bianchi MG Maggini C Gazzola GC Bussolati O 《Amino acids》2006,31(2):93-99
Summary. We report here that chlorpromazine, a first generation antipsychotic drug, inhibits anionic amino acid transport mediated
by system X−
AG (EAAT transporters) in cultured human fibroblasts. With 30 μM chlorpromazine, transport inhibition is detectable after 3 h
of treatment, maximal after 48 h (>60%), and referable to a decrease in Vmax. Chlorpromazine effect is not dependent upon changes of membrane potential and is selective for system X−
AG since transport systems A and y+ are not affected. Among antipsychotic drugs, the inhibitory effect of chlorpromazine is shared by two dibenzodiazepines,
clozapine and olanzapine, while other compounds, such as risperidon, zuclopentixol, sertindol and haloperidol, are not effective.
Transport inhibition by clozapine and olanzapine, but not by chlorpromazine, is reversible, suggesting that the mechanisms
involved are distinct. These results indicate that a subset of antipsychotic drugs inhibits EAAT transporters in non-nervous
tissues and prompt further investigation on possible alterations of glutamate transport in peripheral tissues of schizophrenic
patients. 相似文献
7.
Summary. Although there are a great number of studies concerning the uptake of taurine in several tissues, the regulation of taurine
transport has not been studied in the retina after lesioning the optic nerve. In the present study, isolated retinal cells
of the goldfish retina were used either immediatly after cell suspension or in culture. The high-affinity transport system
of [3H]taurine in these cells was sodium-, temperature- and energy-dependent, and was inhibited by hypotaurine and β-alanine, but
not by γ-aminobutyric acid. There was a decrease in the maximal velocity (Vmax) without modifications in the substrate affinity (Km) after optic axotomy. These changes were mantained for up to 15 days after the lesion. The results might be the summation
of mechanisms for providing extracellular taurine to be taken up by other retinal cells or eye structures, or regulation by
the substrate taurine, which increases after lesioning the optic nerve. The in vivo accumulation of [3H]taurine in the retina after intraocular injection of [3H]taurine was affected by crushing the optic nerve or by axotomy. A progressive retinal decrease in taurine transport was
observed after crushing the optic nerve, starting at 7 hours after surgery on the nerve. The uptake of [3H]taurine by the tectum was compensated in the animals that were subjected to crushing of the optic nerve, since the concentration
of [3H]taurine was only different from the control value 24 hours after the lesion, indicating an efficient transport by the remaining
axons. On the contrary, the low levels of [3H]taurine in the tectum after axotomy might be an index of the non-axonal origin of taurine in the tectum. Axonal transport
was illustrated by the differential presence of [3H]taurine in the intact or crushed optic nerve. The uptake of [3H]taurine into retinal cells in culture in the absence or in the presence of taurine might indicate the existence of an adaptive
regulation of taurine transport in this tissue, however taurine transport probably differentially occurs in specific populations
of retinal cells. The use of a purified preparation of cells might be useful for future studies on the modulation of taurine
transport by taurine in the retina and its role during regeneration.
Received June 11, 1999/Accepted August 31, 1999 相似文献
8.
Summary. We have recently reported that the nitric oxide (NO) donor, sodium nitroprusside (SNP), induces seizures which are associated
with an increase in the basal release of aspartate and glutamate from rat hippocampus (Kaku et al., 1998). In order to determine
whether taurine release occurs with SNP-induced seizures, we examined the effects of NO-related compounds, i.e., the NO trapper,
diethyldithiocarbamate (DETC), the superoxide radical scavenger, dithiothreitol (DTT), the xanthine oxidase inhibitor, oxypurinol
and the guanylyl cyclase inhibitor, 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one (ODQ), on SNP-induced seizures and in vivo taurine release from rat hippocampus using microdialysis. Perfusion with 0.5 mM SNP provoked seizures and significantly increased
taurine release, with the increase in release occurring primarily during reperfusion with artificial cerebrospinal fluid lacking
SNP. Perfusion with 5 mM DETC significantly abolished the SNP-induced seizures and reduced taurine release during and after
perfusion with the drugs. Perfusion with 1 mM DTT significantly reduced both the frequency of the SNP-induced seizures and
taurine release during and after perfusion with the drugs. Perfusion with 1 mM oxypurinol or 0.5 mM ODQ did not reduce the
frequency of the SNP-induced seizures, but tended to decrease taurine release during and after perfusion with the drugs. These
results demonstrate that SNP-induced seizures are triggered by an increase in both NO and peroxynitrite and are related to
an increase in taurine release from rat hippocampus.
Received January 25, 2000/Accepted January 31, 2000 相似文献
9.
Mühling J Nickolaus KA Matejec R Langefeld TW Harbach H Engel J Wolff M Weismüller K Fuchs M Welters ID Krüll M Heidt MC Hempelmann G 《Amino acids》2008,34(2):257-270
We examined the effects of beta-alanine (taurine analogue and taurine transport antagonist), taurine (regarding its role in neutrophil (PMN) immunonutrition) and taurine combined either with L-NAME (inhibitor of *NO-synthase), SNAP (*NO donor), DON (glutamine-analogue and inhibitor of glutamine-requiring enzymes), DFMO (inhibitor of ornithine-decarboxylase) and beta-alanine on neutrophil amino- and alpha-keto acid profiles or important PMN immune functions in order to establish whether taurine transport-, nitric oxide-, glutamine- or ornithine-dependent mechanisms are involved in any of the taurine-induced effects. According to the present findings, the taurine-mediated effect appears to be based primarily on a modulation of important transmembraneous transport mechanisms and only secondarily on directly or indirectly induced modifications in intragranulocytic amino- and alpha-keto acid homoeostasis or metabolism. Although a direct relation to the parallel observed immunological modifications can only be presumed, these results show very clearly that compositional modifications in the free intragranulocytic amino- and alpha keto-acid pools coinciding with changes in intragranulocytic taurine levels are relevant metabolic determinants that can significantly influence the magnitude and quality of the granulocytic immune response. 相似文献
10.
Summary. This paper examines a unique hypothesis regarding an important role for taurine in renal development. Taurine-deficient neonatal
kittens show renal developmental abnormalities, one of several lines of support for this speculation. Adaptive regulation
of the taurine transporter gene is critical in mammalian species because maintenance of adequate tissue levels of taurine
is essential to the normal development of the retina and the central nervous system. Observations of the remarkable phenotypic
similarity that exists between children with deletion of bands p25-pter of chromosome 3 and taurine-deficient kits led us
to hypothesize that deletion of the renal taurine transporter gene (TauT) might contribute to some features of the 3p-syndrome.
Further, the renal taurine transporter gene is down-regulated by the tumor suppressor gene p53, and up-regulated by the Wilms
tumor (WT-1) and early growth response-1 (EGR-1) genes. It has been demonstrated using WT-1 gene knockout mice that WT-1 is
critical for normal renal development. In contrast, transgenic mice overexpressing the p53 gene have renal development defects,
including hypoplasia similar to that observed in the taurine-deficient kitten. This paper reviews evidence that altered expression
of the renal taurine transporter may result in reduced intracellular taurine content, which in turn may lead to abnormal cell
volume regulation, cell death and, ultimately, defective renal development.
Received January 25, 2000/Accepted January 31, 2000 相似文献
11.
Summary. In the kidney the proximal tubule is responsible for the uptake of amino acids. This occurs via a variety of functionally
and structurally different amino acid transporters located in the luminal and basolateral membrane. Some of these transporters
show an ion-dependence (e.g. Na+, Cl− and K+) or use an H+-gradient to drive transport. Only a few amino acid transporters have been cloned or functionally characterized in detail
so far and their structure is known, while little is known about a majority of amino acid transporters. Only few attempts
have been untertaken looking at the regulation of amino acid transport. We summarized more recent information on amino acid
transport in the renal proximal tubule emphasizing functional and regulatory aspects.
Received August 8, 1999; Accepted April 20, 2000 相似文献
12.
13.
Summary. Hepatocytes were cultured for 3 days as spheroids (aggregates) or as monolayers in basal medium and in sulfur amino acid-supplemented
media. Cultured hepatocytes had low levels of cysteine dioxygenase (CDO) activity and normal levels of γ-glutamylcysteine
synthetase (GCS) and cysteinesulfinate decarboxylase (CSDC) activities compared to freshly isolated cells. CDO activity increased
and GCS activity decreased in a dose-response manner in cells cultured in either methionine- or cysteine-supplemented media.
CSDC activity was not significantly affected by methionine supplementation. Changes in CDO and GCS were associated with changes
in cysteine catabolism to taurine plus sulfate and in synthesis of glutathione, respectively. These responses are similar
to those observed in liver of intact rats fed diets supplemented with sulfur amino acids. A near-maximal response of CDO or
GCS activity was observed when the medium contained 1.0 mmol/L of methionine plus cyst(e)ine. Changes in CDO and GCS activities
did not appear to be mediated by changes in the intracellular glutathione concentration. Cultured hepatocytes offer a useful
model for further studies of cysteine metabolism and its regulation in response to sulfur amino acid availability.
Received June 2, 1999/Accepted September 16, 1999 相似文献
14.
Summary. The aim of this study was to evaluate the effect of endotoxin on PMN leukocyte respiratory burst activity by measuring G6PD,
NADPH oxidase and XO activities in guinea pig. In addition, the possible protective role of taurine against endotoxin-mediated
PMN leukocyte function was examined. All experiments were performed with four groups (control, taurine, endotoxemia, taurine
plus endotoxin) of ten guinea pigs. After the endotoxin was administrated (4 mg/kg) both G6PD and NADPH oxidase activities
were significantly reduced compared with the control group. NADPH oxidase activity returned to the control value and G6PD
activity also increased but it did not reach the control value. However when taurine was administrated (300 mg/kg) the activity
of NADPH oxidase reached the control value; furthermore, G6PD activity also increased but it could not reach to the control
value. When taurine was administrated alone, no effect on these enzymes was observed. Following the endotoxin administration,
the activity of XO considerably increased. When taurine was administrated together with endotoxine and alone, this activity
decreased compared to control value in both conditions. These results indicate that the O2
•− formation in PMN leukocytes after the endotoxin administration is ensured by the catalysis of XO due to the inhibited NADPH
oxidase activity. It was observed that taurine has considerable anti-inflammatory and antioxidant effects. However, conflicting
results were obtained when taurine was administrated alone or together with an oxidant agent. 相似文献
15.
Summary. The effects of chronic taurine treatment on the reactivity of the aorta form male Wistar-Kyoto rats were investigated. Contractile
responses to norepinephrine (NE) and potassium chloride (KCl) were attenuated in aortic rings from taurine-treated rats as
compared to controls both in the absence and presence of endothelium. However, the degree of attenuation was greater in endothelium-intact
tissues contracted with NE. Acetylcholine (Ach)-induced relaxation responses were augmented in endothelium-intact vessels
from rats supplemented with taurine compared to the responses observed in control preparations. Relaxation responses of the
aortae from control and taurine-treated rats to sodium nitroprusside (SNP) were not different from each other. Our results
suggest that taurine treatment attenuates vascular contractility nonspecifically and this effect is partly mediated via the
endothelium.
Received December 20, 1999/Accepted January 9, 2000 相似文献
16.
Summary. In the literature taurine is characterized as a non-specific growth or blood clotting factor, an antioxidant, a membrane
protector, or a regulator of calcium ion homeostasis, just as vitamins A, D, E, F, and K are similarly characterized. On the
basis of recent finding concerning the relationship between taurine and the aldehyde of vitamin A-retinal (Petrosian and Haroutounian,
1988, 1998; Petrosian et al., 1996), as well as on the basis of data from the literature, we now suggest a hypothesis that
taurine promotes the bioavailability of the lipid soluble vitamins A, D, E, K, and F, probably by forming different types
of water soluble, easily hydrolyzable complexes. It is quite possible that the ability of taurine to convert lipids and lipid
soluble substances into a water soluble state is the key to understanding the unusually wide diversity of biological phenomena
associated with taurine. This form of delivery may be an additional, secondary mechanism for the transport of lipid soluble
vitamins, which was probably acquired early in evolution, and remains extremely important for mammals and humans directly
after birth for a variety of physiological functions such as: vision in normal and in emergency situations, rapid blood clotting,
sperm eruption, and situations requiring a prompt consumption of lipid soluble vitamins characteristic of excitable systems.
Clearly, the role of taurine in the physiology of the water insoluble vitamins remains an enigma and is worthy of further
investigations.
Received December 23, 1999; Accepted December 28, 1999 相似文献
17.
Summary. Red Bull energy drink has become extraordinarily popular amongst college students for use as a study aid. We investigated
the combined effects of Red Bull’s two active ingredients, caffeine and taurine, on short term memory. Studies on the effects
of these two neuromodulators on memory have yielded mixed results, and their combined actions have not yet been investigated.
In this double-blind study, college student subjects consumed either caffeine and taurine pills or a placebo and then completed
a memory assessment. Heart rate and blood pressure were monitored throughout the testing period. The combination of caffeine
and taurine had no effect on short term memory, but did cause a significant decline in heart rate and an increase in mean
arterial blood pressure. The heart rate decline may have been caused by pressure-induced bradycardia that was triggered by
caffeine ingestion and perhaps enhanced by the actions of taurine. 相似文献
18.
Summary. Previously we have observed the lack of immunoreactivity of taurine in the rod outer segments from light-adapted fish, such
as the ayu Plecoglossus altivelis and lefteye flounder Paralichthys olivaceus. This finding prompted us to investigate if there is a difference in the immunocytochemical localization of taurine in the
rod outer segments between the dark- and light-adapted states. In the retinas of the glass eel Anguilla japonica and the young goldfish Carassius auratus, extremely intense immunostaining was found in the cone outer segments, rod inner segments, photoreceptor supranuclear region
and outer plexiform layer. The rod outer segments were not immunostained in the light-adapted state, while they were intensely
immunostained in the dark-adapted state. Consequently, it was suggested that the lack of immunoreactivity in the rod outer
segment may depend on light stimulation. In addition, the conspicuous immunocytochemical localization of taurine was discussed
with the possible functional roles for taurine in the fish retina.
Received January 25, 2000/Accepted January 31, 2000 相似文献
19.
Summary. Taurine has been thought to function as a regulator of neuronal activity, neuromodulator and osmoregulator. Moreover, it is
essential for the development and survival of neural cells and protects them under cell-damaging conditions. Taurine is also
involved in many vital functions regulated by the brain stem, including cardiovascular control and arterial blood pressure.
The release of taurine has been studied both in vivo and in vitro in higher brain areas, whereas the mechanisms of release
have not been systematically characterized in the brain stem. The properties of release of preloaded [3H]taurine were now characterized in slices prepared from the mouse brain stem from developing (7-day-old) and young adult
(3-month-old) mice, using a superfusion system. In general, taurine release was found to be similar to that in other brain
areas, consisting of both Ca2+-dependent and Ca2+-independent components. Moreover, the release was mediated by Na+-, Cl−-dependent transporters operating outwards, as both Na+-free and Cl− -free conditions greatly enhanced it. Cl− channel antagonists and a Cl− transport inhibitor reduced the release at both ages, indicating that a part of the release occurs through ion channels.
Protein kinases appeared not to be involved in taurine release in the brain stem, since substances affecting the activity
of protein kinase C or tyrosine kinase had no significant effects. The release was modulated by cAMP second messenger systems
and phospholipases at both ages. Furthermore, the metabotropic glutamate receptor agonists likewise suppressed the K+-stimulated release at both ages. In the immature brain stem, the ionotropic glutamate receptor agonists N-methyl-D-aspartate
(NMDA) and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) potentiated taurine release in a receptor-mediated manner.
This could constitute an important mechanism against excitotoxicity, protecting the brain stem under cell-damaging conditions. 相似文献
20.
Effects of Taurine on Calcium Ion Uptake and Protein Phosphorylation in Rat Retinal Membrane Preparations 总被引:5,自引:3,他引:2
J. B. Lombardini 《Journal of neurochemistry》1985,45(1):268-275
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. 相似文献