介绍一种重要的氨基酸—牛磺酸

<正> 牛磺酸是生物界分布很广的一种氨基酸。这种氨基酸的氨基在β-位,酸基为磺酸基,所以牛磺酸的化学命名是β-氨基乙(基)磺酸或2-氨基乙(基)磺酸(H_2N·CH_2·CH_2·SO_3H),属含硫氨基酸。牛磺酸的化学性质稳定,溶于水,不溶于乙醇和乙醚,分子量为125。早在1827年就知道生物体中有牛磺酸,不过对它的代谢和生理功能知道的不多,因     

氨基酸自动分析仪测定血浆中牛磺酸程序的改进及其应用

<正> 牛磺酸是一种由胱氨酸转化而来的β—氨基酸。已有研究证实,牛磺酸与生长发育、体温调节、营养作用、学习记忆及某些疾病有关。由于牛磺酸具有调节生理功能的作用,目前牛磺酸代谢方面的     

熊胆汁中氨基酸与牛磺酸的分析

<正> 本文报道了用氨基酸自动分析仪对熊胆汁中牛磺酸及氨基酸进行分析的方法,并对天然熊胆汁与人工引流熊胆汁中牛磺酸及氨基酸含量的差异情况进行了研究。黑熊(Selenarctos thibetanus)系属哺乳纲(Mammalia)食肉目(Carnivora(熊科(Ursidae)动物,我国多数地区均有     

牛磺酸对人脑神经细胞增殖,分化影响的研究

牛磺酸(taurine,C_2H_7NO_3S)的发现至今已有150多年的历史,但对它在动物体内生理功能的认识,还是在近20年内的研究中积累起来的。牛磺酸是一种结构简单,但在体内具有广泛生理功能的β-氨基酸。与其他参与蛋白质合成的氨基酸不同,通常它不做为蛋     

牛磺酸对运动大鼠血清脂质的影响

牛磺酸对运动大鼠血清脂质的影响侯香玉,李维根,高云秋（北京医科大学运动医学研究所北京１０００８３）牛磺酸属于含硫的β－氨基酸,是细胞内主要的自由氨基酸,具有调节细胞渗透压、细胞内钙离子浓度和稳定细胞质膜等广泛的生物学效应。为研究牛磺酸对运动机体的作用...     

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。     

用DANS反应-聚酰胺薄膜层析-荧光方法对小鼠尾壳核γ-氨基丁酸和牛磺酸的超微量测定

本工作将DANS反应和微量薄膜层析技术与荧光测量加以修改后联用,并注意了组织样品的去蛋白和DANS-牛磺酸洗脱剂的改进,获得了满意的定量测定氨基酸的结果。GABA、牛磺酸的浓度(GABA:0—60×10~(-12)克分子;牛磺酸:0—300×10~(-12)克分子)与其相应的DANS衍生物的荧光强度成线性关系。回收率分别为95—113％和82—94％。灵敏度比原有荧光方法提高了近100倍(10~(-12)克分子数量级)。用此法测得小鼠尾壳核中的GABA和牛磺酸分别为1.26±0.06和15.5±1.0微克分子/克湿重,组织样品只需0.5毫克或更少些。这为测定微量神经组织中的自由氨基酸提供了一种简便的超微量方法.     

天然珍珠母液及其配方产品实验结果的分析

目的研究分析天然珍珠母液中主要的微量化学成分及其配方产品。方法采用《中华人民共和国国家标准》中的食品氨基酸、牛磺酸和微量元素及化妆品的测定方法进行检测。结果天然珍珠母液富含人体所需的氨基酸、牛磺酸和多种微量元素,具有无致病菌及重金属不超标和产品获得认证的特点。结论天然珍珠母液有潜在的多领域应用和综合开发价值。     

牛磺酸对急性运动后血清心肌酶的影响

牛磷酸是一种β—氨基酸的亚磺酸类似物,长期被认为是含硫氨基酸的无功能终末代谢产物。80年代开始,Huxtable等对牛磺酸的分布、代谢及其重要而广泛的生物学作用进行了深入的研究,尤其在牛磺酸对心血管系统的保护作用的研究方面,取得了一定的成果。为探讨急性运动时牛磺酸对心脏的作用,我们观察了牛磺酸对急性运动后血清心肌酶活性的影响。     

Xterra RP18柱高效液相色谱法快速分离测定氨基酸

建立了一种用XterraRP1 8色谱柱快速分离测定水解氨基酸的方法。所采用的色谱条件是 :WatersAlliance系统 ,柱温 5 6℃ ,流速 1 .8ml/min ,检测波长 2 4 8nm ,梯度分离 ,运行周期 2 5min,柱反压低于 2 0 0 0Psi。在 1 7.5min内分离了包括AMQ、NH3 和牛磺酸在内的 2 1种氨基化合物 ,适应于复合氨基酸注射液、含牛磺酸的氨基酸口服液及水解氨基酸样品的分析测定     

Taurine enhancement of calcium binding to rat heart sarcolemma.

The effect of taurine on calcium binding to isolated rat heart sarcolemmal membrane was examined. Taurine was observed to increase calcium binding to the low affinity sites in both high sodium-low potassium and low sodium-high potassium buffers. Taurine was also seen to antagonize the inhibition of calcium binding to the sarcolemma caused by both verapamil and lanthanum. Nevertheless, membrane structural changes due to taurine could not be detected using the spin label ESR probe 2N14. A possible regulatory role of taurine is discussed.     

Purification and structural characterization of polybrominated biphenyl congeners.

Two sets of taurine receptors on rat heart sarcolemma have been identified. The high affinity taurine receptors (Kd=3.5×10^?4M) show a non-cooperative binding profile while the low affinity taurine receptors exhibit positive cooperativity. Taurine binding to the membrane exhibits a typical bell shaped pH profile with maximum binding occurring at pH 8.0. The maximum temperature for binding is 24°C. The effect of various taurine analogues on the receptors was investigated. It was found that binding is prevented by hypotaurine and inhibited to a lesser degree by isethionic acid and cysteine sulfinic acid, while β-alanine was found to increase taurine binding. The effect of several hydrolytic enzymes was also examined and it was shown that several proteases and phospholipase C inhibit binding. The results indicate that the taurine receptors are membrane bound proteins in a phospholipid environment.     

Taurine and Its Chloramine: Modulators of Immunity

Taurine is a semiessential amino acid that is not incorporated into proteins. In mammalian tissues, taurine is ubiquitous and is the most abundant free amino acid in the heart, retina, skeletal muscle, and leukocytes. Taurine reaches up to 50 mM concentration in leukocytes. Taurine has been shown to be tissue-protective in many models of oxidant-induced injury. One possibility is that taurine reacts with HOCl, produced by the myeloperoxidase (MPO) pathway, to produce the more stable but less toxic taurine chloramine (Tau-Cl). However, data from several laboratories demonstrate that Tau-Cl is a powerful regulator of the immune system. Specifically, Tau-Cl has been shown to downregulate the production of proinflammatory mediators in both rodent and human leukocytes. Recent molecular studies on the function of taurine provide evidence that taurine is a constituent of biological macromolecules. Specifically, two novel taurine-containing modified uridines have been found in both human and bovine mitrochondria. In studies on mechanism of action, Tau-Cl inhibits the activation of NFkappaB, a potent signal transducer for inflammatory cytokines, by oxidation of IkappaB alpha at methionine45. Taurine transporter knockout mice show reduced taurine, reduced fertility, and loss of vision resulting from severe retinal degeneration, which was found to be due to apoptosis. Apoptosis induced by amino chloramines is a current and important finding because oxidants derived from leukocytes play a key role in killing pathogens. The fundamental importance of taurine in adaptive and acquired immunity will be revealed using genetic manipulation.     

Na+-Dependent Transport of Taurine by Membrane Vesicles of Neuroblastoma ± Glioma Hybrid Cells

The transport of taurine into membrane vesicles prepared from neuroblastoma x glioma hybrid cells 108CC5 was studied. A great part of the taurine uptake by the membrane preparation is due to the transport into an osmotically sensitive space of membrane vesicles. Taurine uptake by membrane vesicles is an active transport driven by the concentration gradient of Na+ across the membrane (outside concentration greater than inside). The Km value of 36 microM for Na+-dependent taurine uptake indicates a high-affinity transport system. The rate of taurine transport by the membrane vesicles is enhanced by the K+ gradient (inside concentration greater than outside) and the K+ ionophore valinomycin. Taurine transport is inhibited by several structural analogs of taurine: hypotaurine, beta-alanine, and taurocyamine. All these results indicate that the taurine transport system of the membrane vesicles displays properties almost identical to those of intact neuroblastoma X glioma hybrid cells.     

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.     

Effect of taurine on ischemia–reperfusion injury

Taurine is an abundant β-amino acid that regulates several events that dramatically influence the development of ischemia–reperfusion injury. One of these events is the extrusion of taurine and Na⁺ from the cell via the taurine/Na⁺ symport. The loss of Na⁺ during the ischemia–reperfusion insult limits the amount of available Na⁺ for Na⁺/Ca²⁺ exchange, an important process in the development of Ca²⁺ overload and the activation of the mitochondrial permeability transition, a key process in ischemia–reperfusion mediated cell death. Taurine also prevents excessive generation of reactive oxygen species by the respiratory chain, an event that also limits the activation of the MPT. Because taurine is an osmoregulator, changes in taurine concentration trigger “osmotic preconditioning,” a process that activates an Akt-dependent cytoprotective signaling pathway that inhibits MPT pore formation. These effects of taurine have clinical implications, as experimental evidence reveals potential promise of taurine therapy in preventing cardiac damage during bypass surgery, heart transplantation and myocardial infarction. Moreover, severe loss of taurine from the heart during an ischemia–reperfusion insult may increase the risk of ventricular remodeling and development of heart failure.     

Taurine distribution in rat tissues during development.

1. Taurine levels have been determined in eight rat organs. 2. During postnatal growth the taurine content in retina, heart, small intestine, spleen and lung increases with advancing age, although adult values are not reached at the same time. 3. In contrast the taurine content decreases with age in brain cortex, liver and kidney. 4. The taurine in subcellular fractions of adult, 20-day-old and 5-day-old rat tissues exists predominantly in the cytosol of the cell. Taurine content in particulate fractions shows marked variations during development in the different organs. 5. Taurine distribution in the subcellular fractions suggests that some of the cellular taurine in the tissues is not freely mobile in cytosol.     

Regulation of taurine transport in Ehrlich ascites tumor cells

Summary Taurine influx is inhibited and taurine efflux accelerated when the cell membrane of Ehrlich ascites tumor cells is depolarized. Taurine influx is inhibited at acid pH partly due to the concomitant depolarization of the cell membrane partly due to a reduced availability of negatively charged free carrier. These results are in agreement with a 2Na, 1Cl, 1taurine cotransport system which is sensitive to the membrane potential due to a negatively charged empty carrier. Taurine efflux from Ehrlich cells is stimulated by addition of LTD4 and by swelling in hypotonic medium. Cell swelling in hypotonic medium is known to result in stimulation of the leukotriene synthesis and depolarization of the cell membrane. The taurine efflux, activated by cell swelling, is dramatically reduced when the phospholipase A₂ is inhibited indirectly by addition of the anti-calmodulin drug pimozide, or directly by addition of RO 31-4639. The inhibition is in both cases lifted by addition of LTD₄. The swelling-induced taurine efflux is also inhibited by addition of the 5-lipoxygenase inhibitors ETH 615-139 and NDGA. It is concluded that the swelling-induced activation of the taurine leak pathway involves a release of arachidonic acid from the membrane phospholipids and an increased oxidation of arachidonic acid into leukotrienes via the 5-lipoxygenase pathway. LTD₄ seems to act as a second messenger for the swelling induced activation of the taurine leak pathway either directly or indirectly via its activation of the Cl^– channels, i.e., via a depolarization of the cell membrane.     

Taurine level in the blood and myocardium of rabbits with experimental heart failure

Experimental damage of the aortal heart valve in rabbits caused taurine accumulation in the heart. Taurine content in the heart increased for two months 2.7 times in the left ventricle and 1.8 times in the right one. Taurine concentration in the blood began rising 5-10 days after the operation, reached the maximal value of about 150% as compared with its initial level and then decreased to the level near the initial one. Animals with insignificant taurine accumulation in the heart died for the first two months after the operation. Results are discussed from consideration on the protective role of taurine for the myocardium under the heart failure.     

Age-Related Retinal Degeneration in Animal Models of Aging: Possible Involvement of Taurine Deficiency and Oxidative Stress

There is strong evidence that the retina degenerates with age. Electroretinogram deficits and photoreceptor cell death and structural abnormalities have been observed in both animal and human studies of aging. The mechanism behind this phenomenon is a very interesting area for scientific and medical study. Current data support the link between retinal degeneration and increased oxidative stress. Taurine is a free amino acid found in high millimolar concentrations in the retina, and age-related deficiency in retinal levels of taurine may contribute to the retinal degeneration associated with age. Taurine acts as an antioxidant and taurine replenishment is known to alleviate oxidative stress in the retina. Thus taurine supplementation may be useful in the treatment of age-related retinal dysfunction.