牛磺酸对自发性高血压大鼠血压及其心,脑,肾脂质过氧化损伤的影响

牛磺酸对自发性高血压大鼠血压及其心、脑、肾脂质过氧化损伤的影响李辉,李俭春,江时森（南京军区总医院心脏科南京２１０００２）近年研究发现,牛磺酸具有降压、抗心律失常、抗动脉粥样硬化等多种作用,但其确切机制尚不清楚。本研究观察了牛磺酸对自发性高血压大鼠（...     

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。     

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     

牛磺酸研究进展

牛磺酸具有抗肿瘤、增强免疫、保护心脏、降压、降血脂、降血糖、减轻脂肪肝、降转氨酶、抗衰老等诸多作用。本文查阅国内外相关文献,并将其分析归纳,综述了牛磺酸性质、药理作用的研究进展,以为含有牛磺酸的守宫及含守宫中成药的抗肿瘤等临床作用机理提供研究线索。     

牛磺酸研究进展

牛磺酸具有抗肿瘤、增强免疫、保护心脏、降压、降血脂、降血糖、减轻脂肪肝、降转氨酶、抗衰老等诸多作用。本文查阅国内外相关文献,并将其分析归纳,综述了牛磺酸性质、药理作用的研究进展,以为含有牛磺酸的守宫及含守宫中成药的抗肿瘤等临床作用机理提供研究线索。     

牛磺酸对学习记忆影响的研究现状

牛磺酸作为一种条件必须氨基酸对学习记忆能力的影响受到越来越多的关注,许多研究证明适量牛磺酸的添加可明显提高大鼠的记忆能力。通过牛磺酸对神经细胞、基因、激素、离子、受体、酶类等的作用,对其影响学习记忆方面的研究现状作出综述。     

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。     

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。     

植物中存在牛磺酸

<正> 牛磺酸(2-氨基乙磺酸)存在于动物几乎所有器官中,其在机体中所起的重要作用日益受到重视。但就植物而言,仅在某些海藻中发现有少量牛磺酸存在。至于植物中磺酸含量和生理作用尚待阐明。因此,我们用新近开发的电子捕获气相色谱法作了实验研究,证实植物中存在牛磺酸并测定了其含量。     

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。     

High expression of the taurine transporter TauT in primary cilia of NIH3T3 fibroblasts

Taurine, present in high concentrations in various mammalian cells, is essential for regulation of cell volume, cellular oxidative status as well as the cellular Ca2+ homeostasis. Cellular taurine content is a balance between active uptake through the saturable, Na(+)-dependent taurine transporter TauT, and passive release via a volume-sensitive leak pathway. Here we demonstrate that: (i) TauT localizes to the primary cilium of growth-arrested NIH3T3 fibroblasts, (ii) long-term exposure to TNF(alpha) or hypertonic sucrose medium, i.e., growth medium supplemented with 100 mM sucrose, increases ciliary TauT expression and (iii) long-term exposure to hypertonic taurine medium, i.e., growth medium supplemented with 100 mM taurine, reduces ciliary TauT expression. These results point to an important role of taurine in the regulation of physiological processes located to the primary cilium.     

Taurine and β-alanine intraperitoneal injection in lactating mice modifies the growth and behavior of offspring

Taurine, one of the sulfur-containing amino acids, has several functions in vivo. It has been reported that taurine acts on γ-aminobutyric acid receptors as an agonist and to promote inhibitory neurotransmission. Milk, especially colostrum, contains taurine and it is known that milk taurine is essential for the normal development of offspring. β-Alanine is transported via a taurine transporter and a protein-assisted amino acid transporter, the same ones that transport taurine. The present study aimed to investigate whether the growth and behavior of offspring could be altered by modification of the taurine concentration in milk. Pregnant ICR mice were separated into 3 groups: 1) a control group, 2) a taurine group, and 3) a β-alanine group. During the lactation periods, dams were administered, respectively, with 0.9% saline (10?ml/kg, i.p.), taurine dissolved in 0.9% saline (43 mg/10?ml/kg, i.p.), or β-alanine dissolved in 0.9% saline (31 mg/10?ml/kg, i.p.). Interestingly, the taurine concentration in milk was significantly decreased by the administration of β-alanine, but not altered by the taurine treatment. The body weight of offspring was significantly lower in the β-alanine group. β-Alanine treatment caused a significant decline in taurine concentration in the brains of offspring, and it was negatively correlated with total distance traveled in the open field test at postnatal day 15. Thus, decreased taurine concentration in the brain induced hyperactivity in offspring. These results suggested that milk taurine may have important role of regulating the growth and behavior of offspring.     

Swelling-induced taurine transport: relationship with chloride channels, anion-exchangers and other swelling-activated transport pathways.

Cells have to regulate their volume in order to survive. Moreover, it is now evident that cell volume per se and the membrane transport processes which regulate it, comprise an important signalling unit. For example, macromolecular synthesis, apoptosis, cell growth and hormone secretion are all influenced by the cellular hydration state. Therefore, a thorough understanding of volume-activated transport processes could lead to new strategies being developed to control the function and growth of both normal and cancerous cells. Cell swelling stimulates the release of ions such as K(+) and Cl(-) together with organic osmolytes, especially the beta-amino acid taurine. Despite being the subject of intense research interest, the nature of the volume-activated taurine efflux pathway is still a matter of controversy. On the one hand it has been suggested that osmosensitive taurine efflux utilizes volume-sensitive anion channels whereas on the other it has been proposed that the band 3 anion-exchanger is a swelling-induced taurine efflux pathway. This article reviews the evidence for and against a role of anion channels and exchangers in osmosensitive taurine transport. Furthermore, the distinct possibility that neither pathway is involved in taurine transport is highlighted. The putative relationship between swelling-induced taurine transport and volume-activated anionic amino acid, alpha-neutral amino acid and K(+) transport is also examined.     

Taurine transport in human placental trophoblast is important for regulation of cell differentiation and survival

The outer epithelial cell layer of human placenta, the syncytiotrophoblast, is a specialised terminally differentiated multinucleate tissue. It is generated and renewed from underlying cytotrophoblast cells that undergo proliferation, differentiation and fusion with syncytiotrophoblast. Acquisition of fresh cellular components is thought to be balanced by apoptosis and shedding of aged nuclei. This process of trophoblast cell turnover maintains a functional syncytiotrophoblast, capable of sufficient nutrient transfer from mother to foetus. Foetal growth restriction (FGR) is a pregnancy complication associated with aberrant trophoblast turnover and reduced activity of certain amino acid transporters, including the taurine transporter (TauT). Taurine is the most abundant amino acid in human placenta implying an important physiological role within this tissue. Unlike other amino acids, taurine is not incorporated into proteins and in non-placental cell types represents an important osmolyte involved in cell volume regulation, and is also cytoprotective. Here, we investigated the role of taurine in trophoblast turnover using RNA interference to deplete primary human trophoblast cells of TauT and reduce intracellular taurine content. Trophoblast differentiation was compromised in TauT-deficient cells, and susceptibility of these cells to an inflammatory cytokine that is elevated in FGR was increased, evidenced by elevated levels of apoptosis. These data suggest an important role for taurine in trophoblast turnover and cytoprotection.     

Transport, nutritional and metabolic studies of taurine in staphylococci

A specific, Na+-dependent, energy-requiring transport system for taurine has been reported recently in the Staphylococcus aureus M strain. Taurine was taken up vigorously by all S. aureus strains tested. The system was Na+-dependent, and Na+ decreased the Km but had no effect on the Vmax of the transport system. Among coagulase-negative staphylococci, the Staphylococcus epidermidis group (a taxonomically related group of species associated with humans or other primates) and the free-living, wide-ranging species Staphylococcus sciuri showed vigorous taurine uptake. Somewhat lower rates were found in the Staphylococcus saprophyticus group. Low or barely detectable uptake rates were noted in other staphylococcal species that were primarily of animal origin. No taurine uptake was detected in a variety of other bacterial species tested. Taurine uptake, which was not Na+-dependent, occurred in a Pseudomonas aeruginosa strain grown on taurine as sole energy, carbon, nitrogen, and sulphur source, but not when it was grown in a gluconate/salts medium. In nutritional studies we were unable to demonstrate a role for taurine as a sulphur source for S. aureus. [1,2-14C]- and [35S]taurine were taken up during overnight growth of cells, and radioactivity was distributed similarly among cellular fractions, indicating that the carbon and sulphur atoms of taurine were not cleaved and had the same fate. We were unable to demonstrate any catabolism of taurine in radiorespirometric experiments to detect evolution of 14CO2 by cells incubated with [1,2-14C]taurine. Thus, we found no evidence for a role of taurine in the energy, carbon and sulphur metabolism of S. aureus.     

Taurine and inflammatory diseases

Taurine (2-aminoethanesulfonic acid) is the most abundant free amino acid in humans and plays an important role in several essential biological processes such as bile acid conjugation, maintenance of calcium homeostasis, osmoregulation and membrane stabilization. Moreover, attenuation of apoptosis and its antioxidant activity seem to be crucial for the cytoprotective effects of taurine. Although these properties are not tissue specific, taurine reaches particularly high concentrations in tissues exposed to elevated levels of oxidants (e.g., inflammatory cells). It suggests that taurine may play an important role in inflammation associated with oxidative stress. Indeed, at the site of inflammation, taurine is known to react with and detoxify hypochlorous acid generated by the neutrophil myeloperoxidase (MPO)–halide system. This reaction results in the formation of less toxic taurine chloramine (TauCl). Both haloamines, TauCl and taurine bromamine (TauBr), the product of taurine reaction with hypobromous acid (HOBr), exert antimicrobial and anti-inflammatory properties. In contrast to a well-documented regulatory role of taurine and taurine haloamines (TauCl, TauBr) in acute inflammation, their role in the pathogenesis of inflammatory diseases is not clear. This review summarizes our current knowledge concerning the role of taurine, TauCl and TauBr in the pathogenesis of inflammatory diseases initiated or propagated by MPO-derived oxidants. The aim of this paper is to show links between inflammation, neutrophils, MPO, oxidative stress and taurine. We will discuss the possible contribution of taurine and taurine haloamines to the pathogenesis of inflammatory diseases, especially in the best studied example of rheumatoid arthritis.     

The taurine transporter gene and its role in renal development

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     

Deletion of the γ-Aminobutyric Acid Transporter 2 (GAT2 and SLC6A13) Gene in Mice Leads to Changes in Liver and Brain Taurine Contents

The GABA transporters (GAT1, GAT2, GAT3, and BGT1) have mostly been discussed in relation to their potential roles in controlling the action of transmitter GABA in the nervous system. We have generated the first mice lacking the GAT2 (slc6a13) gene. Deletion of GAT2 (both mRNA and protein) neither affected growth, fertility, nor life span under nonchallenging rearing conditions. Immunocytochemistry showed that the GAT2 protein was predominantly expressed in the plasma membranes of periportal hepatocytes and in the basolateral membranes of proximal tubules in the renal cortex. This was validated by processing tissue from wild-type and knockout mice in parallel. Deletion of GAT2 reduced liver taurine levels by 50%, without affecting the expression of the taurine transporter TAUT. These results suggest an important role for GAT2 in taurine uptake from portal blood into liver. In support of this notion, GAT2-transfected HEK293 cells transported [³H]taurine. Furthermore, most of the uptake of [³H]GABA by cultured rat hepatocytes was due to GAT2, and this uptake was inhibited by taurine. GAT2 was not detected in brain parenchyma proper, excluding a role in GABA inactivation. It was, however, expressed in the leptomeninges and in a subpopulation of brain blood vessels. Deletion of GAT2 increased brain taurine levels by 20%, suggesting a taurine-exporting role for GAT2 in the brain.     

Human placental taurine transporter in uncomplicated and IUGR pregnancies: cellular localization, protein expression, and regulation

Transplacental transfer is the fetus' primary source of taurine, an essential amino acid during fetal life. In intrauterine growth restriction (IUGR), placental transport capacity of taurine is reduced and fetal taurine levels are decreased. We characterized the protein expression of the taurine transporter (TAUT) in human placenta using immunocytochemistry and Western blotting, tested the hypothesis that placental protein expression of TAUT is reduced in IUGR, and investigated TAUT regulation by measuring the Na(+)-dependent taurine uptake in primary villous fragments after 1 h of incubation with different effectors. TAUT was primarily localized in the syncytiotrophoblast microvillous plasma membrane (MVM). TAUT was detected as a single 70-kDa band, and MVM TAUT expression was unaltered in IUGR. The PKC activator PMA and the nitric oxide (NO) donor 3-morpholinosydnonimine decreased TAUT activity (P < 0.05, n = 7-15). However, none of the tested hormones, e.g., leptin and growth hormone, altered TAUT activity significantly. PKC activity measured in MVM from control and IUGR placentas was not different. In conclusion, syncytiotrophoblast TAUT is strongly polarized to the maternal-facing plasma membrane. MVM TAUT expression is unaltered in IUGR, suggesting that the reduced MVM taurine transport in IUGR is due to changes in transporter activity. NO release downregulates placental TAUT activity, and it has previously been shown that IUGR is associated with increased fetoplacental NO levels. NO may therefore play an important role in downregulating MVM TAUT activity in IUGR.     

Cloning,tissue and ontogenetic expression of the taurine transporter in the flatfish Senegalese sole (Solea senegalensis)

Flatfish species seem to require dietary taurine for normal growth and development. Although dietary taurine supplementation has been recommended for flatfish, little is known about the mechanisms of taurine absorption in the digestive tract of flatfish throughout ontogeny. This study described the cloning and ontogenetic expression of the taurine transporter (TauT) in the flatfish Senegalese sole (Solea senegalensis). Results showed a high similarity between TauT in Senegalese sole and other vertebrates, but a change in TauT amino acid sequences indicates that taurine transport may differ between mammals and fish, reptiles or birds. Moreover, results showed that Senegalese sole metamorphosis is an important developmental trigger to promote taurine transport in larvae, especially in muscle tissues, which may be important for larval growth. Results also indicated that the capacity to uptake dietary taurine in the digestive tract is already established in larvae at the onset of metamorphosis. In Senegalese sole juveniles, TauT expression was highest in brain, heart and eye. These are organs where taurine is usually found in high concentrations and is believed to play important biological roles. In the digestive tract of juveniles, TauT was more expressed in stomach and hindgut, indicating that dietary taurine is quickly absorbed when digestion begins and taurine endogenously used for bile salt conjugation may be recycled at the posterior end of the digestive tract. Therefore, these results suggest an enterohepatic recycling pathway for taurine in Senegalese sole, a process that may be important for maintenance of the taurine body levels in flatfish species.