从生产半胱氨酸的废母液中回收胱氨酸的工艺研究

研究了一种从生产半胱氨酸的废母液中回收胱氨酸的工艺,介绍了工艺过程并讨论了其主要原理及影响因素。该方法工艺简单,操作方便,对设备的要求低,而回收率、产品含量均较高,是一种回收利用氨基酸、减少环境污染的好方法。     

氨基酸母液中含盐量的测定方法探讨

本文采用不同氯离子（Ｃｌ－）含量的测定方法（摩尔法、电位滴定法、氯离子选择性电极法）,探讨出适用于猪毛水解提取胱氨酸后的未脱盐氨基酸母液（简称母液Ⅰ）、脱盐氨基酸母液（简称母液Ⅱ）以及由母液Ⅱ经浓缩结晶出的固体氨基酸粉末中的Ｃｌ－含量测定的最佳方法。     

D-半胱氨酸盐酸盐制备研究

D-半胱氨酸盐是手性药物,主要是第三代头孢抗生素药物—头孢米诺钠的重要中间体。本文介绍了D-半胱氨酸盐酸盐的研制。采用L-半胱氨酸盐酸盐为出发原料,经消旋、沉淀异构体、结晶分离、提纯的方法,制成达到日本味之素公司1997年公布的产品质量指标的D-半胱氨酸盐酸盐。     

电渗析法分离提纯N-乙酰-L-半胱氨酸研究

使用我校由辐射法制备的高性能离子交换膜ＨＦ—１及ＨＦ—２,采用电渗析技术对合成所得的Ｎ－乙酰－Ｌ－半胱氨酸进行了分离提纯,脱盐率＞１５％,损失率＜１５％,为工业化应用提供了依据。     

猪毛中胱氨酸的分离和复合氨基酸的制备

本文研究了以猪毛为原料,经过水解、赶酸、中和、结晶、精制提取出胱氨酸纯品;并从分离胱氨酸后的母液中,经过脱色、离子交换、浓缩、结晶、精制,制备出复合氨基酸.在本工艺条件下,胱氨酸产品的收率为4.8%,纯度在99%以上;复合氨基酸产品的收率为41%,纯度在83%以上.本文为扩大试验打下了基础.     

利用毛发水解提取胱氨酸后的废液研制氨基酸复合肥料

利用胱氨酸废液中游离氨基酸为主要成份研制氨基酸肥料,既解决了废液排放问题,又开辟了新的肥料来源。本文详尽叙述这一研制的工艺原则流程,强调添加剂在这一流程中的作用,并对氨基酸肥料的肥效进行了试验研究。     

利用葡萄糖废母液生产酒精的研究

选育出两株利用葡萄糖废母液生产酒精的菌株S_(995)和S_8。S_(095)用于70％母液和30％糖蜜混合连续酒精发酵,醪液中酒精份平均可达10.1％。S_8用于50％、70％母液和50％、30％玉米糖化醪混合生产酒精,醪液中酒精份可达12.37％(实验室数据)和10％(实际生产数据)。     

由人发制备胱氨酸的工艺研究

实验对胱氨酸的生产流程作了进一步的探讨 ,讨论了原料的用量、酸度、水解时间、水解温度及收得率的最佳条件 ,在提高生产工艺的同时 ,降低生产成本。     

Effects of ATP and Taurine on Calcium Uptake by Membrane Preparations of the Rat Retina

Abstract: The effects of ATP and taurine on the kinetics of calcium uptake in rat retinal membrane preparations were determined. ATP increased calcium uptake at low calcium ion concentrations. Addition of ATP plus taurine further increased calcium uptake. Cooperative relationships were observed for calcium uptake in the absence of ATP and taurine. In the presence of phosphate ions reciprocal plots demonstrated upward deflections from linear ty, while in the absence of phosphate ions downward deflections were noted. Addition of ATP plus taurine to the incubation system appeared to obliterate the cooperativity. Two uptake systems for calcium were observed.     

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。     

Photochemical Damage in the Albino Rat Retina: Oral Taurine Has No Effect on DNA and Protein Loss from Severely Damaged Photoreceptor Cells

Albino Wistar rats were exposed continuously to fluorescent light, causing photoreceptor destruction over a period of 4 days. The rate of DNA and protein loss from the cells was not affected by administration of 5% taurine in the drinking water.     

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%。     

牛磺酸对虎纹蛙非特异性免疫及血清氧化还原状态的影响

为探讨牛磺酸在无尾两栖类免疫调节和抗氧化能力方面的功能和作用,通过灌胃方式研究了不同浓度牛磺酸对虎纹蛙(Hoplobatrachus rugulosus)脾巨噬细胞呼吸爆发、外周血吞噬活力、胃溶菌酶活力以及血清丙二醛(MDA)和谷胱甘肽(GSH)含量的影响。结果表明:连续7 d的牛磺酸灌胃可显著提高脾巨噬细胞的呼吸爆发强度和外周血细胞的吞噬活力并呈现出明显的剂量效应。当灌胃浓度达到0.8 g/L时两者均达到峰值,但高于0.8 g/L时则表现出条件毒性。胃溶菌酶活力在各浓度下无明显变化。此外,血清MDA含量随牛磺酸浓度的升高而降低,GSH含量在一定的浓度范围内呈现出明显的剂量效应,在1 g/L时达到峰值。研究结果证明牛磺酸可以明显提高虎纹蛙的非特异性免疫功能和机体氧化防御能力,但摄入过量则表现出条件毒性。基于上述指标的评估,虎纹蛙对牛磺酸的适宜需求量按体重计算约为16~20 mg/kg。     

A Possible Role for Taurine in Osmoregulation Within the Brain

Intracranial microdialysis was used to measure changes in extracellular amino acids within the rat brain during local osmotic alteration of the extracellular microenvironment or during systemic water intoxication. Increased cellular hydration produced by either of these methods was accompanied by a marked increase in extracellular taurine levels without affecting the other amino acids measured. With local osmotic alteration, this increase was osmolarity dependent and reversible. The specificity, sensitivity, and reversibility of the increase in extracellular taurine strongly suggest a functional role in osmoregulation in the brain under normal as well as pathological 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.     

Effects of mercury on myosin ATPase in the ventricular myocardium of the rat

Mercury reduces twitch and tetanic force development in isolated rat papillary muscles, and a putative toxic effect on the contractile machinery has been suggested. Based on that, the actions of HgCl2 on the myosin ATPase activity of the left ventricular myocardium were investigated. Samples for assay of myosin ATPase activity were obtained from rats' left ventricles. Increasing concentrations of HgCl2 reduced dose-dependently the activity of the myosin ATPase. This reduction was observed even at very small concentrations, 50 nM HgCl2. This effect was dependent on the presence of SH groups in the myosin molecule since DTT and glutathione protected the myosin ATPase against toxic effects of mercury; full activity being restored by using 500 nM DTT or 500 nM glutathione. Results also suggested that the metal acts as an uncompetitive inhibitor with a Ki of 200 nM HgCl2. Our results suggest that mercury reduces the activity of the myosin ATPase by an uncompetitive mechanism at a very low dose that does not depress force. DTT and glutathione are effective for protection against the actions of mercury suggesting that SH groups might be the sites of action of the metal on the myosin molecule.     

Effects of Taurine on Calcium Ion Uptake and Protein Phosphorylation in Rat Retinal Membrane Preparations

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.     

Inactive to active transitions of the mitochondrial ATPase complex as controlled by the ATPase inhibitor

The hydrolytic and phosphorylation activities of the ATPase complex of bovine heart mitochondria are regulated by the ATPase inhibitor of Pullman and Monroy [1]. The inhibiting action of the peptide on ATPase activity can be overcome by a proton-motive force. Submitochondrial particles that contain the inhibitor, either intrinsically or externally added, show a lag that precedes phosphorylation. Particles devoid of the inhibitor, or particles that are in an ‘active’ state fail to present the lag. Accordingly, the data indicate that, prior to the onset of phosphorylation, the ATPase complex undergoes a transition to an active state through a process that involves the inhibitor. The transition depends on the concentration of ATP, 50 μM ATP giving 50% inhibition of the proton-motive force-induced transition.