荧光法测定蒜头果蛋白中Trp的含量

蒜头果蛋白(malanin)是从蒜头果种仁中分离、纯化出的一种新的植物蛋白质.以Na OH为水解液水解malanin,在激发波长225 nm,发射波长350 nm处测定色氨酸(Trp)的相对荧光强度.结果表明,malanin中Trp的含量为5.116 mg·g-1,即每分子malanin中含Trp约为4个.此结果将为酸水解测定malanin氨基酸的组成作为补充,同时也为malanin全序列的测定提供较好的参考数据.     

对二甲氨基苯甲醛分光光度法测定色氨酸

在酸性溶液中,色氨酸与对二甲氨基苯甲醛反应生成蓝色缩合物,在595nm波长下有最大吸收,色氨酸样品的浓度在0～12μg.mL-1范围内呈线性关系.实验给出最佳测定条件.     

L-色氨酸-高锰酸钾-H~ 化学发光反应的研究

在酸性条件下，高锰酸钾能直接氧化Ｌ－色氨酸并产生较强的化学发光信号，发光信号的强度与Ｌ－色氨酸浓度在一定范围内成线性，由此建立了Ｌ－色氨酸－高锰酸钾－Ｈ＋化学发光体系测定Ｌ－色氨酸的流动注射化学发光新方法．方法的检出限为２．８×１０－７ｇ／ｍＬＬ－色氨酸，线性范围１．０×１０－６～８．０×１０－５ｇ／ｍＬ．试验了常见氨基酸及糖对Ｌ－色氨酸测定的干扰情况，方法已用于１８氨基酸注射液内Ｌ－色氨酸含量测定     

色氨酸生物合成的多目标稳态优化

研究了色氨酸生物合成的多目标稳态优化.根据已建立的色氨酸生物合成过程模型,采用IOM方法,把多目标非线性优化问题转化为多目标线性优化问题来解决.在保证色氨酸产率的基础上,同时也使代谢物的浓度达到最低.仿真结果表明了优化算法的实用性和有效性.     

N-乙酰基-DL-2-甲基-色氨酸的合成

以丁烯－2－酮，乙酰氨基丙二酸二乙酯以及苯肼为原料合成了非天然的N－乙酰基－DL－2－甲基－色氨酰，产物经核磁、质谱鉴定。     

菘蓝色氨酸合成酶基因的克隆与生物信息学分析

对菘蓝色氨酸合成酶基因IiTSA进行克隆,并对其进行生物信息学分析.结果表明:菘蓝IiTSA基因全长2 111bp,包含8个外显子和7个内含子;cDNA全长1 035bp,编码311个氨基酸,编码的蛋白定位在叶绿体基质中,是一种无信号肽和跨膜结构域的疏水性蛋白;二级结构主要由α-螺旋、β-转角、延伸链和不规则卷曲组成;序列比对结果显示,菘蓝IiTSA核酸序列和氨基酸序列与其他多种植物的TSA核酸序列和氨基酸序列均具有较高的同源性.     

谷氨酸棒状杆菌发酵色氨酸的工艺研究

为了优化发酵工艺,提高色氨酸产量,本文对发酵培养基的碳氮源、发酵条件、及小试发酵过程控制进行了实验研究。结果表明,最佳发酵培养基为葡萄糖4g/L、胰蛋白胨20g/L,色氨酸产量达0.43g/L;在摇瓶发酵的基础上,进一步在50L发酵罐中进行小试表明,在发酵温度36℃、pH7.0、搅拌速率700r/min的条件下,色氨酸产量达0.45g/L。     

聚乙二醇-400胶束介质中的色氨酸流体室温燐光

详细研究了用I-作重原子微扰剂、亚硫酸钠为除氧剂及聚乙二醇-400存在下的胶束增稳室温燐光法测定色氨酸体系.最大激发/发射波长278/440nm,线性范围8.0×10-8～1.0×10-5mol/L.直接用于大米、花生、大豆及竹笋中色氨酸的测定,相对标准偏差2.26%～3.05%,与荧光法比较,相对误差-3.91%～2.86%.     

聚乙二醇-400胶束介质中的色氨酸流体室温燐光

详细研究了用I-作重原子微扰剂、亚硫酸钠为除氧剂及聚乙二醇-400存在下的胶束增稳室温燐光法测定色氨酸体系．最大激发／发射波长２７８／４４０nm,线性范围8.0×10-8～1.0×10-5mol/L.直接用于大米、花生、大豆及竹笋中色氨酸的测定,相对标准偏差2.26%～3.05%,与荧光法比较,相对误差-3.91%～2.86%.     

Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease

Half a century ago, chronic granulomatous disease (CGD) was first described as a disease fatally affecting the ability of children to survive infections. Various milestone discoveries have since been made, from an insufficient ability of patients' leucocytes to kill microbes to the underlying genetic abnormalities. In this inherited disorder, phagocytes lack NADPH oxidase activity and do not generate reactive oxygen species, most notably superoxide anion, causing recurrent bacterial and fungal infections. Patients with CGD also suffer from chronic inflammatory conditions, most prominently granuloma formation in hollow viscera. The precise mechanisms of the increased microbial pathogenicity have been unclear, and more so the reasons for the exaggerated inflammatory response. Here we show that a superoxide-dependent step in tryptophan metabolism along the kynurenine pathway is blocked in CGD mice with lethal pulmonary aspergillosis, leading to unrestrained Vgamma1(+) gammadelta T-cell reactivity, dominant production of interleukin (IL)-17, defective regulatory T-cell activity and acute inflammatory lung injury. Although beneficial effects are induced by IL-17 neutralization or gammadelta T-cell contraction, complete cure and reversal of the hyperinflammatory phenotype are achieved by replacement therapy with a natural kynurenine distal to the blockade in the pathway. Effective therapy, which includes co-administration of recombinant interferon-gamma (IFN-gamma), restores production of downstream immunoactive metabolites and enables the emergence of regulatory Vgamma4(+) gammadelta and Foxp3(+) alphabeta T cells. Therefore, paradoxically, the lack of reactive oxygen species contributes to the hyperinflammatory phenotype associated with NADPH oxidase deficiencies, through a dysfunctional kynurenine pathway of tryptophan catabolism. Yet, this condition can be reverted by reactivating the pathway downstream of the superoxide-dependent step.