Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asparagine was a superior nitrogen source for clavine-alkaloid production in Claviceps purpurea. Its transport into the cell excedded the cell's biosynthetic need for this amino acid. Asparagine entered the cell without degradation. This disturbed the relative pool sizes of various amino acids resulting in a change in the genetically determined ratio at which amino acids were utilized for protein synthesis. Overproduction of alkaloids (4500 mug.ml-1) may be associated with increased availability of tryptophan because of the enhanced assimilation of asparagine-derived ammonia via glutamine synthetase (EC 6.3.1.2). However, ammonium salts in the fermentation broth led to a depression of the alkaloid yield. Partial replacement of the ammonium salt by aspartic acid elevated alkaloid production.
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PMID:The cellular role of nitrogen in the biosynthesis of alkaloids by submerged culture of Claviceps purpurea (Fr.) Tul. 1 58

1. In the posterior half of the pulvinar of cats anaesthetized with halothane and nitrous oxide, the majority of neurons were fired by ACh released with small electrophoretic currents. In the anterior part of that nucleus, ACh had more variable effects: excitation, depression or none. 2. In comparison with L-glutamate, DL-homocysteic acid and DL-aspartic acid, ACh appeared to be the most potent excitant. 3. ACh-induced discharges were easily and reversibly blocked by low doses of atropine. In most cases, ACh effects could not be blocked selectively by mecamylamine or dihydro-beta-erythroidine. 4. Nicotine failed to mimic ACh, whereas carbachol was a potent excitant and was readily blocked by low doses of atropine. 5. The histochemical reaction to acetylcholinesterase was moderate in the pulvinar. 6. These observations support the view that pulvinar cells differ from other thalamic cells.
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PMID:Micro-electrophoretic studies in the cat pulvinar region: effect of acetylcholine. 2 59

A lethal protein with hemagglutinating activity but without trypsin inhibitory activity was isolated from beans of Phaseolus vulgaris, cultiva, and Kintoki and proved homogeneous by ultracentrifugation, disc polyacrylamide gel electrophoresis, sodium dodesyl sulfate polyacrylamide gel electrophoresis and isoelectric focusing. The molecular weight was estimated to be 104, 000 by ultracentrifugal analysis and gel filtration on Sephadex G-200. The molecule dissociates into three identical subunits in the presence of 8 M urea or 0.1% sodium dodesyl sulfate. The amino acid composition was characterized by the high content of aspartic acid and the complete absence of methionine and cystine. The carbohydrate content was 8.1%; 5.0% mannose and 3.1% glucosamine. The addition of the lethal protein to a basal diet (0.4%) resulted in the intensive depression of the growth and finally in the death of rats. The intraperitoneal injection of 250 microgram per g body weight of mouse brought about an acute toxicity which caused death of all the injected mice.
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PMID:The isolation and characterization of a lethal protein from Kintoki beans (Phaseolus vulgaris). 61 Nov 61

We have previously shown that subcutaneous administration of aspartic acid (a dicarboxylic acidic amino acid) at a dose of 580 mg/kg causes long lasting depression of ventilation in adult intact and postpubertally castrated male rats, but not in intact female rats. The purpose of the present study was to determine if hypogonadism induced by perinatal administration of testosterone propionate (TP) will alter ventilation, oxygen consumption, and the ventilatory response to aspartic acid and to hypercapnia in adult males. TP treatment resulted in adult males who had lower body, prostate, heart, and testes weights than those of control male rats. Ventilation in air and oxygen consumption were comparable between the two groups as was the ventilatory response to aspartic acid. In contrast, TP-treated rats exhibited a significantly decreased ventilatory response to hypercapnia due predominantly to lower tidal volumes compared to control animals. Aspartic acid treatment did not affect oxygen consumption in either group. Thus, TP treatment results in the development of adult male rats who, although hypogonadal, retain a male-like ventilatory response to aspartic acid, but whose response to hypercapnia is more like that of hypogonadal men and rats.
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PMID:Control of ventilation in androgenized hypogonadal male rats. 152 34

Previously we observed that acute subcutaneous administration of aspartic acid (580 mg/kg) depressed ventilation in awake male, but not female, rats, suggesting that this agent may be used as a marker for sexual dimorphism in the control of ventilation. Moreover, males castrated postpubertally showed a response similar to that of intact male rats. Thus the hormonal milieu of male rats appear not to be necessary to elicit the masculine type of ventilatory response to aspartic acid. The purpose of this study was 1) to determine whether adult female rats androgenized by the administration of testosterone propionate (TP) 1 day after birth would alter their ventilation in response to aspartic acid to be more malelike and 2) to compare these results with those of intact (I) and ovariectomized (O) female rats. Minute ventilation and O2 consumption in air and in response to aspartic acid administration were evaluated in awake animals in all three groups. Furthermore the minute ventilation of all rats to a hypercapnic challenge was also evaluated. Ovariectomy resulted in rats increased body weights but decreased weight-corrected ventilation and O2 consumption compared with TP-treated and I animals. Minute ventilation after hypercapnic challenge in the three groups was similar. TP-treated rats responded to aspartic acid administration with a marked depression of ventilation similar to that previously noted in males, whereas neither I nor O rats showed such a response. The depression of ventilation in the TP-treated group in response to aspartic acid was not a consequence of a depression of O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of aspartic acid on control of ventilation in androgenized and ovariectomized female rats. 162 80

An alanine-rich, alpha-helical antifreeze polypeptide (AFP) from the winter flounder and seven analogs with variations in the arrangement of neutral, polar amino acids were synthesized. Circular dichroism studies determined that all of the peptides, except for one containing a proline residue, were essentially 100% alpha-helical. Freezing point depression data, analyzed by three methods, showed that rearrangement of polar residues resulted in moderate to complete loss of anti-freeze activity. It was observed that ice crystals grow as hexagonal bipyramids in dilute solutions, with a constant c to alpha axis ratio of about 3.3. Above a critical threshold concentration, which may depend on the AFP to ice binding constant and reflect the onset of cooperative interactions, growth ceases until the temperature is lowered to the freezing point. We conclude that a specific arrangement of both threonine and asparagine (or aspartic acid) residues is critical for maximal activity and that the AFPs probably bind to the pyramidal faces of ice with a specific orientation. These conclusions are consistent with a recent report (Knight, C. A., Cheng, C. C., and DeVries, A. L. (1991) Biophys. J. 59, 409-418) that a similar AFP adsorbs to the [2021] pyramidal planes of ice in dilute solution.
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PMID:Structure-function relationships in an antifreeze polypeptide. The role of neutral, polar amino acids. 162 10

To investigate the role of glutamic (Glu) and aspartic acid (Asp) in migraine, we measured the plasma amino acids in migraine patients with and without aura, between and during attacks, and compared the profiles with the plasma amino acid profiles of tension headache patients and healthy controls. Between attacks, migraineurs (notably with aura) had substantially higher plasma Glu and Asp levels than did controls and tension headache patients. In addition, patients with migraine without aura showed low plasma histidine levels. During migraine attacks, Glu (and to a lesser extent Asp) levels were even further increased. The results suggest a defective cellular reuptake mechanism for Glu and Asp in migraineurs, and we hypothesize a similar defect at the neuronal/glial cell level, predisposing the brain of migraineurs to develop spreading depression.
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PMID:Neuroexcitatory plasma amino acids are elevated in migraine. 197 2

The effects of single and repeated inhalations of acetaldehyde (AcAl) on spontaneous activity and the metabolisms of cerebral monoamines and neuroactive amino acids were investigated. Both single and repeated inhalations of AcAl induced a significant increase of spontaneous activity at the initial stage followed by the loss of motor activity and coma. The AcAl inhalation-induced central excitement, exhibited by hyperkinesia and occasional jumpings, were found to be more severe following a single administration than by repeated ones. These abnormal behaviors observed following a single administration of AcAl, were accompanied by significant decreases of noradrenaline in the cerebral cortex, brainstem and of dopamine in the brainstem. In addition, it was found that these decreases in catecholamines were associated with significant decreases in the contents of 3-methoxy-4-hydroxyphenylethyleneglycol, 3, 4-dihydroxyphenylacetic acid and homovanillic acid in brain. The contents of aspartic acid in the cerebral cortex and of GABA in the brainstem also showed an increase. On the other hand, animals subjected to the repeated inhalation of AcAl and exhibiting a state of central depression, showed the increase of adrenaline as well as the decrease of GABA in the cerebellum. These results suggest that a single inhalation of AcAl may induce central excitation as well as facilitate the metabolic turnover of cerebral catecholamines, while repeated inhalation of AcAl may result in central depression accompanied by decreased turnover of central catecholamines. Possible involvement of the changes in cerebral aspartic acid and GABA in the exhibition of central effects of AcAl is also suggested.
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PMID:Acetaldehyde-induced alterations in metabolism of monoamines in mouse brain. 256 11

Previous studies from this laboratory have demonstrated that growth of the methylcholanthrene (MCA) sarcoma is dependent on total nitrogen substrate availability in vivo and on the specific amino acids asparagine and glutamine in vitro. This experiment determines whether these two phenomena can be used to selectively depress tumor growth and maintain host carcass. Sixty-two rats were inoculated with sarcoma and were infused for 10 days with isocaloric (60 kcal/day) TPN solutions at 100%, 16%, 10%, and 5% of normal nitrogen levels, either with (W) or isonitrogenously without (WO) the amino acids asparagine, glutamine, aspartic acid, and glutamic acid. W solutions contained 33% of these amino acids. Mean weights of 100 W tumors were significantly greater (p = 0.002) than all other groups. Total body weights minus tumor weights were similar in W versus WO animals at each rate of nitrogen infusion. Mean venous plasma concentrations of asparagine, aspartic acid, glutamine, and glutamic acid were similar in all eight groups. These data indicate that the same degree of tumor depression produced by nitrogen deprivation can also be produced by removal of asparagine, glutamine, and their precursors from nutrient solutions without adverse effects on carcass mass. The mechanisms involved are not readily explained by analysis of venous plasma amino acid concentrations.
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PMID:Influence of total nitrogen, asparagine, and glutamine on MCA tumor growth in the Fischer 344 rat. 289 15

beta-Pyrazol-1-yl-DL-alanine, an uncommon amino acid from plants of the Cucurbitaceae, was fed to mice. Although pyrazole is known to affect the liver enzymes UDP-glucose dehydrogenase, UDP-glucuronyl transferase and UDP-glucuronic acid pyrophosphatase, and also depresses their liver glycogen concentrations, beta-pyrazol-1-ylalanine had no such effects. beta-Pyrazol-1-ylalanine could not be detected in the liver of the experimental animals but was present in the urine. No other change in urinary amino acid content was observed. Studies with [14C]-beta-pyrazol-1-yl-DL-alanine showed the administered amino acid was excreted over a 4-day period, 93% of the compound supplied was recovered. Similar recoveries were obtained with the L-enantiomer from cucumber seed. The metabolic inertness of beta-pyrazol-1-ylalanine was also apparent in experiments involving subcutaneous injection of this compound. Administration of pyrazole confirmed an earlier report of resultant increased activity of liver UDP-glucose dehydrogenase and UDP-glucuronyl transferase, and of the depression of activity of liver UDP-glucuronic acid pyrophosphatase. A concomitant 40% decrease in liver glycogen content was seen. The urine contained a novel metabolite, identified as a peptide conjugate of a pyrazole derivative. Mass spectrometry and p.m.r. spectroscopy indicate that this derivative is 3,4,4-trimethyl-5-pyrazolone. The amino acid constituents are aspartic acid, threonine, serine, glutamic acid, proline, glycine, alanine, valine and leucine. The urine of mice receiving pyrazole contained less free glycine and alanine than controls. From the results, it is concluded that pyrazole is not a catabolite of dietary beta-pyrazol-1-ylalanine but to the contrary, the amino acid is essentially excreted unchanged. Formation of 3,4,4-trimethyl-5-pyrazolone from pyrazole would imply C-methylation, a process that has not been previously observed in a mammalian detoxication context.
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PMID:Metabolism of the amino acid beta-pyrazol-1-ylalanine and its parent base pyrazole. 298 41


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