Glutamic acid is metabolized in the tissues by oxidative deamination ... or by transamination with pyruvate to yield oxaloacetic acid ... which, via alpha-ketoglutarate, enters the citric acid cycle ... .. Quantitatively minor but physiologically important pathways of glutamate metabolism involve decarboxylation to gamma-aminobutyrate (GABA) and amidation to glutamine ... . Decarboxylation to GABA is dependent on pyridoxal phosphate, a coenzyme of glutamic acid decarboxylase ..., as is glutamate transaminase. Vitamin B6-deficient rats have elevated serum glutamate levels and delayed glutamate clearance ... . /Glutamic acid/
Oral dose of 1 g/kg monosodium glutamate given to rats was followed by only a small rise in plasma pyroglutamate levels. No incr of pyroglutamate or glutamate brain levels was observed under these conditions.
Glutamic acid is metabolized in the tissues by oxidative deamination ... or by transamination with pyruvate to yield oxaloacetic acid ... which, via alpha-ketoglutarate, enters the citric acid cycle ... .. Quantitatively minor but physiologically important pathways of glutamate metabolism involve decarboxylation to gamma-aminobutyrate (GABA) and amidation to glutamine ... . Decarboxylation to GABA is dependent on pyridoxal phosphate, a coenzyme of glutamic acid decarboxylase ..., as is glutamate transaminase. Vitamin B6-deficient rats have elevated serum glutamate levels and delayed glutamate clearance ... . /Glutamic acid/
Oral dose of 1 g/kg monosodium glutamate given to rats was followed by only a small rise in plasma pyroglutamate levels. No incr of pyroglutamate or glutamate brain levels was observed under these conditions.
Glutamic acid is metabolized in the tissues by oxidative deamination ... or by transamination with pyruvate to yield oxaloacetic acid ... which, via alpha-ketoglutarate, enters the citric acid cycle ... .. Quantitatively minor but physiologically important pathways of glutamate metabolism involve decarboxylation to gamma-aminobutyrate (GABA) and amidation to glutamine ... . Decarboxylation to GABA is dependent on pyridoxal phosphate, a coenzyme of glutamic acid decarboxylase ..., as is glutamate transaminase. Vitamin B6-deficient rats have elevated serum glutamate levels and delayed glutamate clearance ... . /Glutamic acid/
Monosodium glutamate (MSG) administered intraperitoneally /for 10 days/ at a dose of 4 mg/g bw markedly increase malondialdehyde (MDA) formation in the liver, the kidney and brain of rats. Simultaneous administration of VIT C, VIT E and quercetin to MSG-treated rats significantly reduced this increase in MDA induced by MSG. VIT E reduced lipid peroxidation mostly in the liver followed by VIT C and then quercetin, while VIT C and quercetin showed a greater ability to protect the brain from membrane damage than VIT E. The decreased glutathione (GSH) level elicited by MSG in the three organs corresponded with marked increase in the activity of glutathione-S-transferase (GST). While MSG increased (p < 0.001) the activities of superoxide dismutase and catalase in the liver, it decreased significantly the activities of these enzymes in the kidney and the brain. The three antioxidants were effective at ameliorating the effects of MSG on GSH levels and the enzymes in the three organs examined. While MSG increased the activity of glucose-6-phosphatase in the liver and kidneys of rats (p < 0.001), the activity of the enzyme was abysmally low in the brain. There were marked increases in the activities of alanine aminotransferase, aspartate aminotransferase and gamma-glutamyl transferase in rats treated with MSG. The antioxidants tested protected against MSG-induced liver toxicity significantly. MSG at a dose of 4 mg/g significantly (p < 0.01) induced the formation of micronucleated polychromatic erythrocytes (MNPCEs). Co-treatment of rats with VIT C and quercetin inhibited the induction of MNPCEs by MSG (p < 0.001) ...
L-Glutamic acid and its ammonium, calcium, monosodium and potassium salts were evaluated by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1988. The Committee noted that intestinal and hepatic metabolism results in elevation of levels in systemic circulation only after extremely high doses given by gavage (>30mg/kg body weight). Ingestion of monosodium glutamate (MSG) was not associated with elevated levels in maternal milk, and glutamate did not readily pass the placental barrier. Human infants metabolized glutamate similarly to adults. Conventional toxicity studies using dietary administration of MSG in several species did not reveal any specific toxic or carcinogenic effects nor were there any adverse outcomes in reproduction and teratology studies. Attention was paid to central nervous system lesions produced in several species after parenteral administration of MSG or as a consequence of very high doses by gavage. Comparative studies indicated that the neonatal mouse was most sensitive to neuronal injury; older animals and other species (including primates) were less so. Blood levels of glutamate associated with lesions of the hypothalamus in the neonatal mouse were not approached in humans even after bolus doses of 10 g MSG in drinking water. Because human studies failed to confirm an involvement of MSG in "Chinese Restaurant Syndrome" or other idiosyncratic intolerance, the JECFA allocated an "acceptable daily intake (ADI) not specified" to glutamic acid and its salts. No additional risk to infants was indicated. The Scientific Committee for Food (SCF) of the European Commission reached a similar evaluation in 1991. The conclusions of a subsequent review by the Federation of American Societies for Experimental Biology (FASEB) and the Federal Drug Administration (FDA) did not discount the existence of a sensitive subpopulation but otherwise concurred with the safety evaluation of JECFA and the SCF.
/SRP Idiosyncratic reaction/: No decontamination measures have been reported. No antidotes exist. Supportive measures: Follow with ECG and cardiac evaluation if chest pain persists. Alert patient to avoid foods with MSG.
/HUMAN EXPOSURE STUDIES/ ... A high dose of 2.5 g was tested in 6 healthy controls and 30 asthmatics (7: allergic asthma; 15: intrinsic asthma with intolerance to aspirin; 8: intrinsic asthma with aspirin intolerance, intolerance to alcohol or to food additives). Two patients presented with a mild bronchospasm, occurring 6 to 10 hours after the ingestion. Different mechanisms are discussed. A cholinergic mechanism might be incriminated, either due to stimulation of the synthesis of acetylcholine, or due to a vagal reflex elicited by a reflux esophagitis. However, a high vagal hyperreactivity seems to be needed for the occurrence of asthma. It is concluded that a very small subset of patients with intrinsic asthma might present with an intolerance to monosodium glutamate if high doses are consumed.
/HUMAN EXPOSURE STUDIES/ Monosodium glutamate is widely regarded as the provocative agent in the "Chinese restaurant syndrome," of which flushing is regarded as part of the reaction. Six subjects were monitored by laser Doppler velocimetry for changes in facial cutaneous blood flow during challenge with monosodium glutamate and its cyclization product, pyroglutamate. Additionally, records of patients challenged with monosodium glutamate in the laboratory were reviewed. No flushing was provoked among the twenty four people tested, eighteen of whom gave a positive history of Chinese restaurant syndrome flushing. These results indicate that monosodium glutamate provoked flushing, if it exists at all, must be rare. Monosodium glutamate and its cyclization product, pyroglutamate, may provoke edema and associated symptoms.
Glutamate is absorbed from the gut by an active transport system specific for amino acids. This process is saturable, can be competitively inhibited, and is dependent on sodium ion concentration... . During intestinal absorption, a large proportion of glutamic acid is transaminated and consequently alanine levels in portal blood are elevated. If large amounts of glutamate are ingested, portal glutamate levels increase ... . This elevation results in increased hepatic metabolism of glutamate, leading to release of glucose, lactate, glutamine, and other amino acids, into systemic circulation ... . The pharmacokinetics of glutamate depend on whether it is free or incorporated into protein, and on the presence of other food components. Digestion of protein in the intestinal lumen and at the brush border produces a mixture of small peptides and amino acids; di-and tri-peptides may enter the absorptive cells where intracellular hydrolysis may occur, liberating further amino acids. Defects are known in both amino acid and peptide transport ... .. Glutamic acid in dietary protein, together with endogenous protein secreted into the gut, is digested to free amino acids and small peptides, both of which are absorbed into mucosal cells where peptides are hydrolyzed to free amino acids and some of the glutamate is metabolized. Excess glutamate and other amino acids appear in portal blood. As a consequence of the rapid metabolism of glutamate in intestinal mucosal cells and in the liver, systemic plasma levels are low, even after ingestion of large amounts of dietary protein. /Glutamic acid/
... Intestinal and hepatic metabolism results in elevation of levels in systemic circulation only after extremely high doses given by gavage (>30mg/kg body weight). Ingestion of monosodium glutamate (MSG) was not associated with elevated levels in maternal milk, and glutamate did not readily pass the placental barrier. Human infants metabolized glutamate similarly to adults.
Oral administration of pharmacologically high doses of glutamate results in elevated plasma levels. The peak plasma glutamate levels are both dose and concentration dependent ... . When the same dose (1 g/kg b.w.) of monosodium glutamate (MSG) was administered by gavage in aqueous solution to neonatal rats, increasing the concentration from 2% to 10% caused a five-fold increase in the plasma area under curve; similar results were observed in mice ... . Conversely, when MSG (1.5 g/kg b.w.) was administered to 43-day-old mice by gavage at varying concentrations of 2 to 20% w/v, no correlation could be established between plasma levels and concentration ...
Administration of a standard dose of 1 g/kg b.w. MSG by gavage as a 10% w/v solution resulted in a marked increase of plasma glutamate in all species studied. Peak plasma glutamate levels were lowest in adult monkeys (6 times fasting levels) and highest in mice (12-35 times fasting levels). Age-related differences between neonates and adults were observed; in mice and rats, peak plasma levels and area under curve were higher in infants than in adults while in guinea pigs the converse was observed.
Glutamate is absorbed from the gut by an active transport system specific for amino acids. This process is saturable, can be competitively inhibited, and is dependent on sodium ion concentration... . During intestinal absorption, a large proportion of glutamic acid is transaminated and consequently alanine levels in portal blood are elevated. If large amounts of glutamate are ingested, portal glutamate levels increase ... . This elevation results in increased hepatic metabolism of glutamate, leading to release of glucose, lactate, glutamine, and other amino acids, into systemic circulation ... . The pharmacokinetics of glutamate depend on whether it is free or incorporated into protein, and on the presence of other food components. Digestion of protein in the intestinal lumen and at the brush border produces a mixture of small peptides and amino acids; di-and tri-peptides may enter the absorptive cells where intracellular hydrolysis may occur, liberating further amino acids. Defects are known in both amino acid and peptide transport ... .. Glutamic acid in dietary protein, together with endogenous protein secreted into the gut, is digested to free amino acids and small peptides, both of which are absorbed into mucosal cells where peptides are hydrolyzed to free amino acids and some of the glutamate is metabolized. Excess glutamate and other amino acids appear in portal blood. As a consequence of the rapid metabolism of glutamate in intestinal mucosal cells and in the liver, systemic plasma levels are low, even after ingestion of large amounts of dietary protein. /Glutamic acid/
Ravidomycin V 和相关化合物，例如，FE35A-B在可见光存在下，对各种癌细胞系表现出有效的抗癌活性。氨基糖部分（D-萝卜糖胺与具有中性或支链糖的密切相关的化合物相比，这些分子中的拉维霉素和类似物的效力更高。在拉维霉素 V 生物合成基因簇中，五个假定的基因编码NDP- D-拉维多胺鉴定了生物合成酶。通过分离的酶的活性在体外，据证实ravD，RAVE，ravIM，ravAMT和ravNMT编码TDP- D-葡萄糖合酶，TDP-4-酮-6-脱氧d -葡萄糖-4,6-脱水酶，TDP-4-酮-6-脱氧d -葡萄糖-3,4-酮异构酶，TDP-3-酮-6-脱氧-D-半乳糖-3-氨基转移酶和TDP-3-氨基-3,6-双脱氧-D-半乳糖-N、N-二甲基-转移酶。一锅酶法合成的方案TDP- d -ravidosamine已经被开发出来。此处提供的结果现在为产生TDP- d -ravidosamine
Bio-based N-alkyl-2-pyrrolidones by Pd-catalyzed reductive N-alkylation and decarboxylation of glutamic acid
作者：Free De Schouwer、Sander Adriaansen、Laurens Claes、Dirk E. De Vos
DOI：10.1039/c7gc01829k
日期：——
controversial high-boiling solvents such as N-methyl-2-pyrrolidone and N,N-dimethylformamide in the chemical industry. Recently, N-alkyl-2-pyrrolidones and 5-methyl-N-alkyl-2-pyrrolidones were proposed as attractive alternative solvents for many applications. Here, we report a bio-based two-step chemocatalytic system for the synthesis of a broad range of N-alkyl-2-pyrrolidones starting from glutamic acid
环保法规推动新的更安全，毒性较低的生物基溶剂的查找替换争议的高沸点溶剂，如ñ甲基-2-吡咯烷酮和ñ，ñ在化工行业二甲基甲酰胺。最近，N-烷基-2-吡咯烷酮和5-甲基-N-烷基-2-吡咯烷酮被提议作为许多应用的有吸引力的替代溶剂。在这里，我们报告了一种基于生物的两步化学催化系统，该系统可以从谷氨酸和C 3 -C 5羰基化合物开始合成范围广泛的N-烷基-2-吡咯烷酮。第一步N通过温和且有效的Pd催化的还原性N-烷基化以高产率（＞ 85％）合成了谷氨酸的α-单烷基化衍生物。随后，在惰性气氛下在250℃下热诱导内酰胺化成相应的N-烷基焦谷氨酸，然后Pd催化脱羧，得到N-烷基-2-吡咯烷酮。通过用碱中和N-烷基焦谷氨酸底物，部分抵消了水解降解，导致产率高达82％。最后，两个反应步骤在相同的Pd / Al 2 O 3催化剂下，在不同的气体气氛和温度条件下，通过一锅法成功地结合在一起。
Decarboxylation of a Wide Range of Amino Acids with Electrogenerated Hypobromite
作者：Roman Matthessen、Laurens Claes、Jan Fransaer、Koen Binnemans、Dirk E. De Vos
DOI：10.1002/ejoc.201403112
日期：2014.10
Bromide-assisted electrochemical decarboxylation efficiently produces valuable nitriles in high yields from a wide range of naturally occurring aminoacids in a single step. Bromide salts are used as both redox mediators and supporting electrolytes in a simple one-compartment setup. As demonstrated for lysine, the selectivity of the decarboxylation can be tuned towards nitriles, amines or amides.
Bio-Based Nitriles from the Heterogeneously Catalyzed Oxidative Decarboxylation of Amino Acids
作者：Laurens Claes、Roman Matthessen、Ine Rombouts、Ivo Stassen、Trees De Baerdemaeker、Diederik Depla、Jan A. Delcour、Bert Lagrain、Dirk E. De Vos
DOI：10.1002/cssc.201402801
日期：2015.1
The oxidativedecarboxylation of aminoacids to nitriles was achieved in aqueous solution by in situ halide oxidation using catalytic amounts of tungstate exchanged on a [Ni,Al] layered double hydroxide (LDH), NH4Br, and H2O2 as the terminal oxidant. Both halide oxidation and oxidativedecarboxylation were facilitated by proximity effects between the reactants and the LDH catalyst. A wide range of
在水溶液中，通过催化卤化原位卤化物，使用在[Ni，Al]层状双氢氧化物（LDH），NH 4 Br和H 2 O 2上交换的钨酸盐，将氨基酸氧化成腈作为末端氧化剂。反应物和LDH催化剂之间的邻近效应促进了卤化物的氧化和氧化的脱羧。各种氨基酸的转化率很高，通常> 90％。腈的选择性非常好，经过适当的中和后，该体系可与酰胺，醇，特别是羧酸，胺和胍官能团相容。这种非均相催化系统已成功应用于将淀粉工业中富含蛋白质的副产物转化为有用的生物基含氮化学品。
Host Marking Pheromone (HMP) in the Mexican Fruit Fly Anastrepha ludens
作者：Andrew J. F. Edmunds、Martin Aluja、Fransico Diaz-Fleischer、Bruno Patrian、Leonhard Hagmann
DOI：10.2533/chimia.2010.37
日期：——
Host marking pheromones (HMPs) are used by insects to mark hosts (usually a fruit) where they have already laid eggs. The compounds serve as a deterrent to conspecifics avoiding over-infestation of hosts (i.e. repeated egg-laying into an already occupied/used host). If these
HMPs are sprayed onto commercially valuable fruit they act as deterrents preventing attack by females interested in laying eggs into the valuable commodity. Having no insecticidal or toxic properties, and being natural products (or close derivatives thereof) they could be used as fruit sprays
to replace insecticides, or in combination with other products to improve efficacy. This review discusses the isolation, and synthesis of the HMP of the Mexican fruit fly Anastrepha ludens a feared pest of citrus and mangos in Mexico and Central America. This compound is also recognized
by females of other pestiferous species in the same genus Anastrepha distributed from the Southern USA to Northern Argentina, including many Caribbean Islands. The synthetic HMP was shown to exhibit strong electrophysiological activity against A. ludens and excellent interspecies
cross recognition with other Anastrepha species. Behavioural tests confirmed the HMP deterring effect of the synthetic natural product. Further studies enabled us to drastically simplify the structure of the HMP and obtain a derivative, which we named Anastrephamide, which shows
HMP deterring effects very similar to the natural product in laboratory and field tests. The potential use of such HMP derivatives in a crop protection scenario is briefly discussed.
