沙蛤中牛磺酸的制备研究

以沙蛤提取液中牛磺酸含量为指标,考察乙醇回流法、水煮法和预处理方法,并采用单因素和正交实验法优化工艺条件,确定了沙蛤中提取牛磺酸的最佳工艺。结果:提取牛磺酸的最佳工艺条件为:超声波破碎15 m in,60℃下80%乙醇回流40 m in,该条件下所得牛磺酸质量分数达6.41 mg.g-1原料。结论:超声波破碎与乙醇回流方法相结合,利于牛磺酸溶出,其含量提高26.9%。     

牡蛎精中牛磺酸含量测定

<正> 牡蛎精是从牡蛎中提取的高效滋补药物,根据日本学者研究表明其中起作用的主要成份为牛磺酸,牛磺酸即氨基乙磺酸,分子式为—NH_2—CH_2—CH_2—SO_3H,因其分子中含有游离氨基,故可用氨基酸分析仪进行定性和定量分析,本文报告牛磺酸的实验工作。     

合浦马氏珍珠母液生物活性成分的检测

目的研究合浦马氏珠母贝提取的珍珠母液,对其主要活性成分进行检测分析。方法采用《中华人民共和国国家标准》中的食品氨基酸、牛磺酸和微量元素的测定方法进行检测。结果合浦马氏珠母贝提取的天然珍珠母液含有丰富的活性物质（氨基酸总含量为223．7mg／100ml、牛磺酸总含量为276．4mg／100ml）和多种微量元素（锌、铜、铁、镁、钙等）。结论从马氏珠母贝中提取的天然珍珠母液有潜在的多领域应用和综合开发价值。     

珍珠贝母体中牛磺酸的提取

以珍珠贝母为原料 ,通过细胞自溶破壁 ,使牛黄酸溶出 ,以离子交换树脂法提取纯化溶液中牛磺酸。实验结果表明 :细胞自溶破壁的最佳条件为温度 4 0℃ ,p H5.5,自溶时间 4 0 h;纯化可使牛磺酸量占氨基酸总量的 80 .6%,回收率为 87.5%。     

分光光度法测定地骨皮中牛磺酸含量

用分光光度法测定地骨皮中是否含有牛磺酸。在一定条件下,牛磺酸与乙酰丙酮和甲醛反应生成带色的配合物,建立了测定牛磺酸含量的分光光度法。结果表明,地骨皮中含有牛磺酸,已测定样品1中牛磺酸的质量分数为3.124 mg.g-1,样品2中牛磺酸的质量分数为6.203 mg.g-1,且样品2中的牛磺酸质量分数极显著高于样品1(p<0.01)。研究结果表明,地骨皮中含有牛磺酸,而且分光光度法成本低,干扰少,是测定地骨皮中牛磺酸质量分数的较好方法。     

不同浓度牛磺酸对高糖诱导的猪PK15细胞凋亡的影响及其作用机制

本研究的目的是探索牛磺酸(Tau)在细胞凋亡过程中的抗凋亡作用机制,筛选最佳保护浓度。在高糖诱导猪PK15细胞凋亡的基础上,添加不同浓度的Tau,培养48 h后收集细胞。提取细胞总RNA,实时荧光定量PCR,检测凋亡抑制基因Bcl-2,凋亡促进基因Bax以及Caspase-3的表达。结果显示:实验组细胞均发生不同程度的凋亡,但随着Tau浓度的增加凋亡程度逐渐减轻。荧光定量PCR显示Bax/Bcl-2比值随着Tau的增加逐渐降低,并且在牛磺酸浓度为20 mmol/L同时达到最低值,此时Caspase-3的表达也达到最低值。本研究成功验证了牛磺酸抗细胞凋亡的作用,并筛选出最佳保护浓度为20 mmol/L,为研究牛磺酸在糖尿病研究领域的应用提供依据。     

高糖对培养大鼠心肌细胞牛磺酸转运的影响及其可能机制

目的：观察不同浓度葡萄糖对细胞牛磺酸(taurine)转运功能的影响。方法：在培养的大鼠心肌细胞上,用^3H标记的牛磺酸测定细胞牛磺酸转运和竞争性定量RTPCR测定细胞牛磺酸转运体(TAUT)mRNA含量。结果：不同浓度葡萄糖(10～30mmol/L)孵育,抑制细胞^3H-牛磺酸转运,呈时间依赖性。与对照组比较,高糖(20mmol／L和30mmol／L)使心肌细胞牛磺酸摄入量显著减少,其^3H-牛磺酸转运的最大速率(Vmax)减少,心肌细胞TAUTmRNA含量较对照组减少。结论：高糖抑制心肌细胞牛磺酸转运,这与TAUT的牛磺酸结合位点减少和TAUT基因转录水平下调有关。     

牛磺酸跨膜转运的意义及机制

牛磺酸是正常存在于体内的含硫氨基酸,其跨膜转运对细胞渗透压的维持及细胞内外Ca~(2 )的稳态调节具有重要的作用。心肌细胞膜上存在Na~ /taurine协同转运系统。牛磺酸跨膜转运主要受Na~ 的调控,另外,渗透压、Ca~(2 )和K~ 等亦影响牛磺酸的转运。牛磺酸转运蛋白的克隆为进一步研究牛磺酸跨膜转运的 机制提供了新的手段。     

牛磺酸调节巨噬细胞功能的研究进展

牛磺酸(Taurine)是机体内分布广泛且具有众多生理功能的含硫氨基酸,近年来牛磺酸对慢性炎症性疾病具有潜在的防治功能已得到广泛认可。巨噬细胞是参与慢性炎症的重要免疫细胞,其牛磺酸含量细胞内比细胞外高出约100倍。大量研究集中在补充牛磺酸可明显改善"无菌性炎症"疾病引起的巨噬细胞聚集和炎症反应。该文就牛磺酸体内水平及其变化、摄入安全性以及对巨噬细胞免疫功能的调节等方面的研究进行了综述,以期为牛磺酸免疫营养分子机制的深入研究和功能食品领域的开发提供参考。     

牛磺酸的营养作用

许多证据表明人、猴和猫合成牛磺酸的能力低,在很大程度上依赖膳食供应。当膳食中长期缺少牛磺酸时会造成机体牛磺酸缺乏,血浆中含量及尿中排出量减低。在猫和猴有视网膜变性、超微结构改变及电生理反应异常。近年来也有关于婴幼儿缺乏牛磺酸引起视网膜功能障碍的报道。目前,有些国家已开始用牛磺酸强化婴儿配方奶制品。     

The Relationship Between Taurine and 3-Nitrotyrosine Level of Hepatocytes in Experimental Endotoxemia

It has been proposed that taurine may function as an oxidant in a dose-dependent manner in vivo and in vitro. The present study was carried out to investigate the relationship between taurine concentration and 3-nitrotyrosine level, a stable marker of peroxynitrite action, in hepatocytes of guinea pig in endotoxemia before and after taurine administration. The levels of taurine and 3-nitrotyrosine were measured by HPLC method. In the present study, taurine was low concentration in hepatocytes exposed to endotoxemia. In taurine plus endotoxin treated animals, HPLC analysis showed higher taurine level compared with animals only supplemented with taurine. But 3-nitrotyrosine levels were same in both taurine alone and taurine plus endotoxin groups. In conclusion, taurine is able to prevent the damaging effect of peroxynitrite, at concentration measured in hepatocytes, in our experimental conditions.     

Taurine deficiency,synthesis and transport in the mdx mouse model for Duchenne Muscular Dystrophy

The amino acid taurine is essential for the function of skeletal muscle and administration is proposed as a treatment for Duchenne Muscular Dystrophy (DMD). Taurine homeostasis is dependent on multiple processes including absorption of taurine from food, endogenous synthesis from cysteine and reabsorption in the kidney. This study investigates the cause of reported taurine deficiency in the dystrophic mdx mouse model of DMD. Levels of metabolites (taurine, cysteine, cysteine sulfinate and hypotaurine) and proteins (taurine transporter [TauT], cysteine deoxygenase and cysteine sulfinate dehydrogenase) were quantified in juvenile control C57 and dystrophic mdx mice aged 18 days, 4 and 6 weeks. In C57 mice, taurine content was much higher in both liver and plasma at 18 days, and both cysteine and cysteine deoxygenase were increased. As taurine levels decreased in maturing C57 mice, there was increased transport (reabsorption) of taurine in the kidney and muscle. In mdx mice, taurine and cysteine levels were much lower in liver and plasma at 18 days, and in muscle cysteine was low at 18 days, whereas taurine was lower at 4: these changes were associated with perturbations in taurine transport in liver, kidney and muscle and altered metabolism in liver and kidney. These data suggest that the maintenance of adequate body taurine relies on sufficient dietary intake of taurine and cysteine availability and metabolism, as well as retention of taurine by the kidney. This research indicates dystrophin deficiency not only perturbs taurine metabolism in the muscle but also affects taurine metabolism in the liver and kidney, and supports targeting cysteine and taurine deficiency as a potential therapy for DMD.     

Taurine in toad brain and blood under different conditions of osmolality: An immunohistochemical study

The concentrations of taurine in blood and brain regions of the toadBufo boreas have been measured. Most of these values are considerably lower than those found in mammals. Using an antibody prepared against conjugated taurine, the distribution of taurine in three brain regions of the toad has been visualized. The possible osmoregulatory functions of taurine have been investigated by making toads hyper- or hypo-osmotic in vivo. Induction of hypoosmolality is accompanied by a massive taurine tide in blood plasma, but has no immediate effects upon the taurine concentrations in the brain areas studied. However, histochemical visualization indicates a marked redistribution of taurine between cellular components and extracellular space of brain tissues. This may indicate that taurine has an osmoregulatory function in brain tissue under hypo-osmotic conditions. Hyperosmolality results in no elevation of the taurine concentration in blood plasma of toads, but rather in a very gradual decline of total plasma taurine content over a prolonged time period. Histochemical studies reveal little change in frontal cortex after 1 hour but deeper staining of many neurons in optic lobe accompanied by greater staining in the extracellular fluid. By 3 hours there is a depletion of taurine from all compartments of cerebral cortex tissues. No evidence of any prolonged direct osmoregulatory role for taurine is indicated under hyperosmotic conditions. A possible indirect osmoregulatory function of taurine is discussed.Special issue dedicated to Dr. Claude Baxter.     

Involvement of γ-aminobutyric acid transporter 2 in the hepatic uptake of taurine in rats

Taurine is essential for the hepatic synthesis of bile salts and, although taurine is synthesized mainly in pericentral hepatocytes, taurine and taurine-conjugated bile acids are abundant in periportal hepatocytes. One possible explanation for this discrepancy is that the active supply of taurine to hepatocytes from the blood stream is a key regulatory factor. The purpose of the present study is to investigate and identify the transporter responsible for taurine uptake by periportal hepatocytes. An in vivo bolus injection of [(3)H]taurine into the rat portal vein demonstrated that 25% of the injected [(3)H]taurine was taken up by the liver on a single pass. The in vivo uptake was significantly inhibited by GABA, taurine, β-alanine, and nipecotic acid, a GABA transporter (GAT) inhibitor, each at a concentration of 10 mM. The characteristics of Na(+)- and Cl(-)-dependent [(3)H]taurine uptake by freshly isolated rat hepatocytes were consistent with those of GAT2 (solute carrier SLC6A13). Indeed, the K(m) value of the saturable uptake (594 μM) was close to that of mouse SLC6A13-mediated taurine transport. Although GABA, taurine, and β-alanine inhibited the [(3)H]taurine uptake by > 50%, each at a concentration of 10 mM, GABA caused a marked inhibition with an IC(50) value of 95 μM. The [(3)H]taurine uptake exhibited a significant reduction when the GAT2 gene was silenced. Immunohistochemical analysis showed that GAT2 was localized on the sinusoidal membrane of the hepatocytes predominantly in the periportal region. These results suggest that GAT2 is responsible for taurine transport from the circulating blood to hepatocytes predominantly in the periportal region.     

Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia

Taurine (2-aminoethanesulfonic acid) is a free sulfur-containing β-amino acid which has antioxidant, antiinflammatory and detoxificant properties. In the present study, the role of endotoxemia on peroxynitrite formation via 3-nitrotyrosine (3-NT) detection, and the possible antioxidant effect of taurine in lipopolysaccharide (LPS)-treated guinea pigs were aimed. 40 adult male guinea pigs were divided into four groups; control, endotoxemia, taurine and taurine+endotoxemia. Animals were administered taurine (300 mg/kg), LPS (4 mg/kg) or taurine plus LPS intraperitoneally. After 6 h of incubation, when highest blood levels of taurine and endotoxin were attained, the animals were sacrificed and spleen samples were collected. The amounts of 3-nitrotyrosine and taurine were measured by HPLC, and reactive nitrogen oxide species (NOx) which are stable end products of nitric oxide was measured spectrophotometrically in spleen tissues. LPS administration significantly decreased the concentration of taurine whilst increased levels of 3-NT and NOx compared with control group. It was determined that taurine treatment decreased the levels of 3-nitrotyrosine and NOx in taurine+endotoxemia group. The group in which taurine was administered alone, contradiction to well-known antioxidant effect, taurine caused elevated concentration of 3-NT and NOx. This data suggest that taurine protects spleen against oxidative damage in endotoxemic conditions. However, the effect of taurine is different when it is administered alone. In conclusion, taurine may act as an antioxidant during endotoxemia, and as a prooxidant in healthy subjects at this dose.     

The biochemical basis for the conjugation of bile acids with either glycine or taurine

All animals, except for the placental mammals, conjugate their bile acids exclusively with taurine. However, in certain of the placental mammals, glycine conjugates are also found. The basis for the appearance of glycine conjugation among the placental mammals was investigated. The reaction of choloyl-CoA with glycine and taurine, as catalysed by the soluble fraction from guinea-pig liver, had a high affinity for taurine and a poor affinity for glycine. The predominant synthesis of glycine conjugates in the guinea pig can be related to the fact that guinea-pig liver contains an unusually low concentration of taurine and a high concentration of glycine. Rabbits make exclusively glycine conjugates and their livers also contain low concentrations of taurine. However, the biochemical basis for their glycine conjugation is more straightforward than in the guinea pig in that the soluble fraction from rabbit liver has a high affinity for glycine and a poor affinity for taurine. Alternative-substrate-inhibition studies with glycine and taurine in soluble fractions from guinea-pig and rabbit liver revealed that glycine and taurine were mutually inhibitory. This suggests that there is only one enzyme for glycine and taurine conjugation in these tissues. The soluble fractions from bovine liver and human liver also made both glycine and taurine conjugates and evidence is presented that suggests that there is only one enzyme in these tissues too. Even the rat, which excretes mostly taurine conjugates, could make both glycine and taurine conjugates in vitro. However, in contrast with all of the placental mammals studied, the supernatant fraction from liver of the chicken, and other non-mammals, could not make glycine conjugates even in the presence of very high concentrations of glycine.     

Physiological roles of taurine in heart and muscle

Taurine (aminoethane sulfonic acid) is an ubiquitous compound, found in very high concentrations in heart and muscle. Although taurine is classified as an amino acid, it does not participate in peptide bond formation. Nonetheless, the amino group of taurine is involved in a number of important conjugation reactions as well as in the scavenging of hypochlorous acid. Because taurine is a fairly inert compound, it is an ideal modulator of basic processes, such as osmotic pressure, cation homeostasis, enzyme activity, receptor regulation, cell development and cell signalling. The present review discusses several physiological functions of taurine. First, the observation that taurine depletion leads to the development of a cardiomyopathy indicates a role for taurine in the maintenance of normal contractile function. Evidence is provided that this function of taurine is mediated by changes in the activity of key Ca²⁺ transporters and the modulation Ca²⁺ sensitivity of the myofibrils. Second, in some species, taurine is an established osmoregulator, however, in mammalian heart the osmoregulatory function of taurine has recently been questioned. Third, taurine functions as an indirect regulator of oxidative stress. Although this action of taurine has been widely discussed, its mechanism of action is unclear. A potential mechanism for the antioxidant activity of taurine is discussed. Fourth, taurine stabilizes membranes through direct interactions with phospholipids. However, its inhibition of the enzyme, phospholipid N-methyltransferase, alters the phosphatidylcholine and phosphatidylethanolamine content of membranes, which in turn affects the function of key proteins within the membrane. Finally, taurine serves as a modulator of protein kinases and phosphatases within the cardiomyocyte. The mechanism of this action has not been studied. Taurine is a chemically simple compound, but it has profound effects on cells. This has led to the suggestion that taurine is an essential or semi-essential nutrient for many mammals.     

The Role of Taurine in the Central Nervous System and the Modulation of Intracellular Calcium Homeostasis

The effects of taurine in the mammalian nervous system are numerous and varied. There has been great difficulty in determining the specific targets of taurine action. The authors present a review of accepted taurine action and highlight recent discoveries regarding taurine and calcium homeostasis in neurons. In general there is a consensus that taurine is a powerful agent in regulating and reducing the intracellular calcium levels in neurons. After prolonged L-glutamate stimulation, neurons lose the ability to effectively regulate intracellular calcium. This condition can lead to acute swelling and lysis of the cell, or culminate in apoptosis. Under these conditions, significant amounts of taurine (mM range) are released from the excited neuron. This extracellular taurine acts to slow the influx of calcium into the cytosol through both transmembrane ion transporters and intracellular storage pools. Two specific targets of taurine action are discussed: Na⁺-Ca²⁺ exchangers, and metabotropic receptors mediating phospholipase-C.     

Reciprocal regulation between taurine and glutamate response via Ca<Superscript>2+</Superscript>- dependent pathways in retinal third-order neurons

Although taurine and glutamate are the most abundant amino acids conducting neural signals in the central nervous system, the communication between these two neurotransmitters is largely unknown. This study explores the interaction of taurine and glutamate in the retinal third-order neurons. Using specific antibodies, both taurine and taurine transporters were localized in photoreceptors and Off-bipolar cells, glutamatergic neurons in retinas. It is possible that Off-bipolar cells release juxtaposed glutamate and taurine to activate the third-order neurons in retina. The interaction of taurine and glutamate was studied in acutely dissociated third-order neurons in whole-cell patch-clamp recording and Ca²⁺ imaging. We find that taurine effectively reduces glutamate-induced Ca²⁺ influx via ionotropic glutamate receptors and voltage-dependent Ca²⁺ channels in the neurons, and the effect of taurine was selectively inhibited by strychnine and picrotoxin, but not GABA receptor antagonists, although GABA receptors are present in the neurons. A CaMKII inhibitor partially reversed the effect of taurine, suggesting that a Ca²⁺/calmodulin-dependent pathway is involved in taurine regulation. On the other hand, a rapid influx of Ca²⁺ through ionotropic glutamate receptors could inhibit the amplitude and kinetics of taurine-elicited currents in the third-order neurons, which could be controlled with intracellular application of BAPTA a fast Ca²⁺ chelator. This study indicates that taurine is a potential neuromodulator in glutamate transmission. The reciprocal inhibition between taurine and glutamate in the postsynaptic neurons contributes to computation of visual signals in the retinal neurons.     

Mechanisms of enhanced taurine release under Ca2+ depletion

The sulfur-containing amino acid taurine is an inhibitory neuromodulator in the brain of mammals, as well as a key substance in the regulation of cell volumes. The effect of Ca(2+) on extracellular taurine concentrations is of special interest in the context of the regulatory mechanisms of taurine release. The aim of this study was to characterize the basal release of taurine in Ca(2+)-free medium using in vivo microdialysis of the striatum of anesthetized rats. Perfusion of Ca(2+)-free medium via a microdialysis probe evoked a sustained release of taurine (up to 180 % compared to the basal levels). The Ca(2+) chelator EGTA (1mM) potentiated Ca(2+) depletion-evoked taurine release. The substitution of CaCl(2) by choline chloride did not alter the observed effect. Ca(2+)-free solution did not significantly evoke release of taurine from tissue loaded with the competitive inhibitor of taurine transporter guanidinoethanesulfonate (1mM), suggesting that in Ca(2+) depletion taurine is released by the transporter operating in the outward direction. The volume-sensitive chloride channel blocker diisothiocyanostilbene-2,2'-disulfonate (1mM) did not attenuate the taurine release evoked by Ca(2+) depletion. The non-specific blocker of voltage-sensitive Ca(2+) channels NiCl(2) (0.65 mM) enhanced taurine release in the presence of Ca(2+). CdCl(2) (0.25 mM) had no effect under these conditions. However, both CdCl(2) and NiCl(2) attenuated the effect of Ca(2+)-free medium on the release of taurine. The data obtained imply the involvement of both decreased influx of Ca(2+) and increased non-specific influx of Na(+) through voltage-sensitive calcium channels in the regulation of transporter-mediated taurine release in Ca(2+) depletion.