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PubMed1998

[Effect of L-glutamic acid on the reception of cytokines by HL-60 cells].

L-Glutamic acid at a concentration of 0.1 microM was found to induce differentiation of the cell line of HL-60 promyelocytic leukemia into granulocytes or neutrophils. The HL-60 cells have no specific glutamate-binding sites, but L-glutamic acid influences the reception of several cytokines by these cells. At a concentration of 0.1 microM, L-glutamic acid completely inhibits the high-affinity binding of 125I-labeled human recombinant interleukin-1 beta (Kd = 0.32 nM) to the HL-60 cells, but does not affect their low-affinity binding (Kd = 13.3 nM) and does not change the total number of the IL-1 beta-binding sites. Preincubation of the HL-60 cells with 0.1 microM of L-glutamic acid increases 2.5 times the number of receptors for 125I-labeled human recombinant tumor necrosis factor beta. These results suggest that L-glutamic acid plays an important role in the differentiation of the blood myeloid cells.

Binding, Competitive↗
PubMed2000

Disposition of glutathione conjugates in rats by a novel glutamic acid pathway: characterization of unique peptide conjugates by liquid chromatography/mass spectrometry and liquid chromatography/NMR.

With the advent of liquid chromatography/mass spectrometry and liquid chromatography/NMR, it has become easier to characterize metabolites that were once difficult to isolate and identify. These techniques have enabled us to uncover the existence of an alternate pathway for the disposition of glutathione adducts of several structurally diverse compounds. Studies were carried out using acetaminophen as a model compound to investigate the role of the glutamic acid pathway in disposition of the glutathione adducts. Although the mercapturic acid pathway was the major route of degradation of the glutathione adducts, it was found that the conjugation of the glutathione, cysteinylglycine, and cysteine adducts of acetaminophen with the gamma-carboxylic acid of the glutamic acid was both interesting and novel. The coupling of the glutathione adduct and the products from the mercapturic acid pathway with the glutamic acid led to unusual peptide conjugates. The natures of these adducts were confirmed unequivocally by comparisons with synthetic standards. This pathway (addition of glutamic acids) led to larger peptides, in contrast to the mercapturic acid pathway, in which the glutathione adducts are broken down to smaller molecules. The enzyme responsible for the addition of glutamic acid to the different elements of the mercapturic acid pathway is currently unknown. It is postulated that the gamma-carboxylic acid is activated (perhaps by ATP) before enzymatic addition to the alpha-amino group of cysteine or glutamate takes place. The discovery of these peptide conjugates of acetaminophen represents a novel disposition of glutathione adducts of compounds. The formation of such conjugates may represent yet another pathway by which drugs could produce covalent binding via their reactive intermediates.

Acetaminophen↗
PubMed1992

Effects of quinolinic acid on messenger RNAs encoding somatostatin and glutamic acid decarboxylases in the striatum of adult rats.

The level of expression of mRNAs encoding somatostatin and two isoforms of glutamic acid decarboxylase (Mr 65,000, GAD65 and 67,000, GAD67) was examined by quantitative in situ hybridization histochemistry in the striatum of adult rats after local injections of quinolinic acid. After a 2-week survival period, Nissl strains showed a profound loss of neurons in the injected striata. With a dose of 120 nmol quinolinic acid, the lesioned area was completely devoid of somatostatin mRNA-positive neurons but contained cells expressing nicotinamide adenine dinucleotide-diaphorase activity (a marker of somatostatinergic interneurons in striatum). After 60 nmol of quinolinic acid, the number of neurons expressing somatostatin mRNA in the lesioned area was similar to controls but the level of labeling per neuron was increased. In the lesioned area, labeling for GAD65 mRNA was abolished and labeling for GAD67 mRNA markedly reduced. However, scattered neurons expressing GAD67 mRNA could still be detected. The majority of surviving GABA-ergic neurons expressed immunoreactivity to parvalbumin, a marker for striatal GABA-ergic interneurons. The results show that quinolinic acid induces dose-dependent alterations in the expression of striatal somatostatin mRNA and reveal a relative sparing of GABA-ergic interneurons in the quinolinic acid-lesioned rat striatum.

Acetylcholinesterase↗
PubMed1980

Regulation and glutamic acid decarboxylase during Neurospora crassa conidial germination.

Glutamic acid decarboxylase (GAD) from Neurospora crassa was assayed in dormant and germinating conidia that had been permeabilized by toluene and methanol. N. crassa conidia contained 10 times the GAD activity found in vegetativemycelia. During conidial germination, GAD activity rapidly decreased to low levels before germ tubes appeared. GAD activity in germinating conidia closely followed the decreasing rate of glutamic acid metabolism. Inhibiting protein synthesis partially blocked the decrease in GAD activity, but eliminating exogenous carbon sources did not alter the initial rate of decrease in this enzyme. However, when conidia were incubated for more than 3 h in distilled water, GAD activity began to increase and eventually reached levels comparable to those in dormant conidia. Either GAD was reversibly inactivated or this enzyme could be synthesized from endogenous storage compounds when conidia were incubated in distilled water. These results are consistent with the hypothesis that GAD is a developmentally regulated enzyme that is responsible for catalyzing the first step in the metabolism of the large pool of free glutamic acid during conidial germination.

Aspartate Aminotransferases↗
PubMed2000

[The effects of the receptor antagonist of glutamic acid on the brain tissue of severely scalded rats].

OBJECTIVE: To explore the influence of glutamic acid on burned rat brain tissue and the effects of the receptor antagonist of glutamic acid. METHODS: Rats inflicted with 30% TBSA III degree scalding injury were taken as the model. The water content, K(+), Na(+), Ca(2+), Mg(2+), nitric oxide metabolites (NO(2)(-)/NO(3)(minus sign))concentrations of scalded rat brain were determined at 2, 6, 12 and 24 postburn hours (PBH). Morphological and histochemical studies of the brain tissue were carried out with LM and EM. RESULTS: The water content, Na(+), Ca(2+)and NO(2)(minus sign)/NO(3)(minus sign) concentrations of the brain tissue after scalding injury were higher than those in control group. But intracerebral ATP enzyme decreased postburn. It was found by EM examination that there existed swelling of capillary endothelium, nerve cells and some intracytoplasmic mitochondria. There appeared pinosome on capillary wall. After the administration of receptor antagonist of glutamic acid, D-2-amino-group-7-phosphoenanthate (D-AP7), the brain water content, Na(+), Ca(2+)and NO(2)(-)/NO(3)(-) concentrations in brain tissue, and the capillary wall pinosome decreased, and the swelling of nerve cells ameliorated. CONCLUSION: There might be postburn increased cerebral microvascular permeability, ischemic injury of cerebral tissue cells and the development of brain edema. The postburn alterations in the morphology and metabolism of brain tissue were correlated with the over secretion of glutamic acid. And the excitatory toxic effects of glutamic acid were mediated by its receptor. The receptor antagonist of glutamic acid D-AP7 might ameliorate postburn cerebral injury.

Adenosine Triphosphatases↗
PubMed2001

Enhanced neuronal protection from oxidative stress by coculture with glutamic acid decarboxylase-expressing astrocytes.

Astrocytes expressing glutamic acid decarboxylase GAD67 directed by the glial fibrillary acidic protein promoter were shown to provide enhanced protection of PC12 cells from H(2)O(2) treatment and serum deprivation in the presence of glutamate. In addition, they protected non-differentiated, but not differentiated, embryonic rat cortical neurons from glutamate toxicity. Glutamic acid decarboxylase (GAD)-expressing astrocytes showed increased glutathione synthesis and release compared to control astrocytes. These changes were due to GAD transgene expression, as transient expression of a GAD antisense plasmid resulted in partial suppression of the increase in glutathione release. In addition to the previously demonstrated increases in NADH and ATP levels and lactate release, GAD-expressing astrocytes show increased antioxidant activity, explaining their ability to protect neurons from various injuries.

Animals↗
PubMed1989

Hormone mediated changes of brain glutamic acid system in amino acid imbalance.

The effects of adrenal cortical hormone and thyroxine on brain glutamic acid, gamma-amino butyric acid (GABA) and glutamine were studied in rats fed on the amino acid imbalanced diet (8% casein diet supplemented with 0.3% L-threonine). The studies revealed that the decrease in brain glutamic acid and GABA levels in threonine imbalance was recovered by hydrocortisone supplementation. The increased level of brain glutamine in threonine imbalance could not, however, be reversed by hydrocortisone supplementation. Thyroxine supplementation was found to have no impact on any of the members of glutamic acid family in the brain of rats receiving the threonine-imbalanced diet. It was suggested that the decreased levels of brain glutamic acid and GABA in threonine imbalance were caused by diminished adrenal cortical function and the influence of adrenal cortical hormone could be suggested to reside at the level of formation of both glutamic acid and GABA.

Adrenal Cortex↗
PubMed2000

Free glutamine and glutamic acid increase in human milk through a three-month lactation period.

BACKGROUND: Previous short observational studies on the free amino acid (FAA) content of human milk have shown that glutamine and glutamic acid increase in the first 4 to 6 weeks of life. METHODS: Changes in human milk content of free amino acids (FAAs) was determined at colostrum, 1 month, and 3 months of lactation in 16 healthy lactating women after delivery of full-term infants. Milk was collected at the end of each feeding (hindmilk) during 24 hours. RESULTS: Glutamic acid and taurine were the most abundant FAAs at colostrum. Although taurine remained stable throughout lactation, glutamic acid (the prevalent FAA) and glutamine increased approximately 2.5 and 20 times, respectively, with progressing lactation representing more than 50% of total FAA at 3 months. The content of essential FAA was also stable, so the change in total FAA content was almost entirely due to the changes in glutamic acid and glutamine. CONCLUSIONS: Breast-fed infants are supplied with progressively increasing amounts of glutamine and glutamic acid throughout lactation. The increasing intake of glutamic acid and glutamine could benefit breast-fed infants with molecules that are likely to protect the enteral mucosa and act as neurotransmitters and as a source of nitrogen.

Adult↗
PubMed1981

Chemical heterogeneity in cerebellar Purkinje cells: existence and coexistence of glutamic acid decarboxylase-like and motilin-like immunoreactivities.

Purkinje neurons of the cerebellar cortex from a chemically and morphologically heterogeneous population containing some members that have gamma-aminobutyric acid (GABA), others that have immunoreactivity for motilin, and a small number that have both. The remaining 30-40% of all Purkinje cells have neither of these two neuroactive substances, leaving possibilities for other transmitter candidates. The evidence was compiled from double-staining immunocytochemical procedures performed on single sections of the cerebellum and brain stem in rat, mouse, and monkey. Two polyclonal antibodies were applied in succession, one directed against the midregion and COOH terminus of the 22-amino acid polypeptide motilin and the other against glutamic acid decarboxylase (glutamate decarboxylase; L-glutamate 1-carboxy-lyase, EC 4.1.1.15), the rate-limiting enzyme in the synthesis of the neurotransmitter GABA. The staining combinations employed the immunoperoxidase method, with different chromogens for distinguishing the motilin-like immunoreactivity from glutamic acid decarboxylase immunoreactivity by different colors, or the immunoperoxidase method for one antiserum and immunofluorescence for the other. The locations of both motilin and GABA cell types were mapped. The recognition of motilin in Purkinje cells calls for experimental definition of the role of this substance in the cerebellum and for reevaluation of the roles of Purkinje cells and of GABA in cerebellar function. The significant motilin representation in the flocculus, paraflocculus, and vermis suggests that it may be the Purkinje cell mediative chemical in the vestibular parts of the cerebellum. However, the presence of GABA as well in the same regions indicates that the chemical preference may be at least bimodal.

Animals↗
PubMed2001

Synthesis and pharmacology of 3-isoxazolol amino acids as selective antagonists at group I metabotropic glutamic acid receptors.

Using ibotenic acid (2) as a lead, two series of 3-isoxazolol amino acid ligands for (S)-glutamic acid (Glu, 1) receptors have been developed. Whereas analogues of (RS)-2-amino-3-(3-hydroxy-5-methyl-4-isoxazolyl)propionic acid [AMPA, (RS)-3] interact selectively with ionotropic Glu receptors (iGluRs), the few analogues of (RS)-2-amino-3-(3-hydroxy-5-isoxazolyl)propionic acid [HIBO, (RS)-4] so far known typically interact with iGluRs as well as metabotropic Glu receptors (mGluRs). We here report the synthesis and pharmacology of a series of 4-substituted analogues of HIBO. The hexyl analogue 9 was shown to be an antagonist at group I mGluRs. The effects of 9 were shown to reside exclusively in (S)-9 (K(b) = 30 microM at mGlu(1) and K(b) = 61 microM at mGlu(5)). The lower homologue of 9, compound 8, showed comparable effects at mGluRs, but 8 also was a weak agonist at the AMPA subtype of iGluRs. Like 9, the higher homologue, compound 10, did not interact with iGluRs, but 10 selectively antagonized mGlu(1) (K(b) = 160 microM) showing very weak antagonist effect at mGlu(5) (K(b) = 990 microM). The phenyl analogue 11 turned out to be an AMPA agonist and an antagonist at mGlu(1) and mGlu(5), and these effects were shown to originate in (S)-11 (EC(50) = 395 microM, K(b) = 86 and 90 microM, respectively). Compound 9, administered icv, but not sc, was shown to protect mice against convulsions induced by N-methyl-D-aspartic acid (NMDA). Compounds 9 and 11 were resolved using chiral HPLC, and the configurational assignments of the enantiomers were based on X-ray crystallographic analyses.

Amino Acids↗
PubMed2002

4-Substituted D-glutamic acid analogues: the first potent inhibitors of glutamate racemase (MurI) enzyme with antibacterial activity.

The first potent inhibitors of glutamate racemase (MurI) enzyme that show whole cell antibacterial activity are described. Optically pure 4-substituted D-glutamic acid analogues with (2R,4S) stereochemistry and bearing aryl-, heteroaryl-, cinnamyl-, or biaryl-methyl substituents represent a novel class of glutamate racemase inhibitors. Exploration of the D-Glu core led to the identification of lead compounds (-)-8 and 10. 2-Naphthylmethyl derivative 10 was found to be a potent competitive inhibitor of glutamate racemase activity (K(i) = 16 nM, circular dichroism assay; IC(50) = 0.1 microg/mL high-performance liquid chromatography (HPLC) assay). Thorough structure-activity relationship (SAR) studies led to benzothienyl derivatives such as 69 and 74 with increased potency (IC(50) = 0.036 and 0.01 microg/mL, respectively, HPLC assay). These compounds showed potent whole cell antibacterial activity against S. pneumoniae PN-R6, and good correlation with the enzyme assay. Compounds 69, 74 and biaryl derivative 52 showed efficacy in an in vivo murine thigh infection model against Streptococcus pneumoniae. Data described herein suggest that glutamate racemase may be a viable target for developing new antibacterial agents.

Amino Acid Isomerases↗
PubMed1989

A novel stereospecific synthesis of 14C labeled 1-glutamic acid.

A stereospecific synthesis of 4-14C-1-glutamic acid was completed in five steps from sodium 2-14C-acetate. The morpholine derived enamine of ethyl pyruvate was reacted with ethyl 2-14C-bromoacetate to give after hydrolysis diethyl 4-14C-2-oxoglutarate. The 2-oxoglutarate was reacted with hydroxylamine hydrochloride to give diethyl 4-14C-2-hydroxyiminoglutarate which was then reduced with a LiAlH4, (-)-N-methylephedrine and 3,5-dimethylphenol mixture to give 4-14C-1-glutamic acid. The 4-14C-1-glutamic acid was used in investigations into the biosynthesis of gamma-lactones in sherries.

Carbon Radioisotopes↗
PubMed2006

Efficient production of poly-gamma-glutamic acid by Bacillus subtilis ZJU-7.

A strain with high poly-gamma-glutamic acid (gamma-PGA) production was isolated from fermented bean curd, a traditional Chinese food. The strain was named Bacillus subtilis ZJU-7 according to 16s rDNA sequencing and its taxonomic characters. The culture conditions for gamma-PGA production were evaluated. The most suitable carbon and nitrogen sources were sucrose and tryptone, respectively. Exogenous L-glutamic acid was necessary for gamma-PGA production, and the production of gamma-PGA increased on the addition of L-glutamic acid to the medium. In the medium containing 60 g/L of sucrose, 60 g/L of tryptone, 80 g/L of L-glutamic acid, and 10 g/L of NaCl, the yield of gamma-PGA reached 54.4 g/L after cultivation at 37 degrees C for 24 h, which was the highest gamma-PGA production compared with values reported in the literature. The average molecular mass of gamma-PGA produced was about 1.24 x 106 Daltons. B. subtilis ZJU-7 is genetically stable and can synthesize levan instead of gamma-PGA without the addition of L-glutamic acid to the medium.

Bacillus subtilis↗