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

The possible role of glutamate dehydrogenase, glutamate synthase, and glutamine synthetase in the regulation of enzyme formation in the gamma-aminobutyric acid (GABA) catabolic pathway of Escherichia coli K-12 was investigated. Evidence is presented indicating that glutamine synthetase acts as a positive regulator in the E. coli GABA control system. Mutations impairing glutamate synthase activity prevent the depression of the enzymes of the GABA pathway in ammonia-limited glucose media. However, mutations resulting in constitutive synthesis of glutamine synthetase (GlnC) restore the ability of the glutamate synthase-less mutants to grow in glucose-GABA media and result in depressed synthesis of the GABA enzymes. It is suggested that the loss of glutamate synthesis activity affects the GABA control system indirectly by lowering glutamine synthetase levels.
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PMID:Regulation of gamma-aminobutyric acid degradation in Escherichia coli by nitrogen metabolism enzymes. 2 37

Chronic ammonia toxicity in experimental mice was induced by exposing them for 2 and 5 days to 5 % (v/v) ammonia solution. The enzymes concerned with glutamate metabolism (aspartate-, alanine- and tyrosine aminotransferases, glutamate dehydrogenase and glutamine synthetase) and (Na+ + K+)-ATPase were estimated in the three regions of brain (cerebellum, cerebral cortex and brain stem) and in liver. Glutamate, aspartate, alanine, glutamine and GABA, RNA and protein were also estimated in the three regions of brain and liver. A significant rise in the activity of (Na+ + K+)-ATPase in all the three regions of brain along with a fall in the activity of alanine aminotransferase was noticed. Changes in the activities of other enzymes were also observed. A significant increase in alanine and a decrease in glutamic acid was observed while no change was observed in the content of other amino acids belonging to the glutamate family. As a result of this, changes in the ratios of glutamate/glutamine and glutamate + aspartate/GABA was observed. The results indicated that the brain was in a state of more depression and less of excitation. Under these conditions the liver tissue was showing a profound rise in the activity of the enzymes of glutamate metabolism. The results are further discussed.
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PMID:Chronic metabolic effects of ammonia in mouse brain. 9 19

Myocardial levels of ammonia, glutamate, and glutamine and the release of glutamate and glutamine were studied in the isolated perfused rat heart during perfusion with ammonium chloride, epinephrine, and conditions of anoxia or ischaemia. Perfusion for 15 min with effective ammonium chloride concentrations of 0.53, 0.71, and 2.06 mmol/l resulted in glutamine production of 1.34, 0.95, and 4.41 mmol with 15 min-1/200 dry weight compatible with the presence of glutamine synthetase in rat myocardium. Myocardial ammonium content was unchanged by perfusion with 0.53 and 0.71 mmol/l ammonium chloride, but was increased by 1.36 mumol with 15 min-1/200 mg dry weight by perfusion with 2.06 mmol/l ammonium chloride. Increased myocardial contents of ammonia and glutamine were not accompanied by depression of left ventricular pressure. Perfusion with epinephrine (0.20 mug/ml) resulted in an increased myocardial content of glutamine. Anoxia or ischaemia resulted in no changes in ammonia content, and no changes in glutamine or glutamate production. The net release of glutamine into the perfusate was about 10 times the net release of glutamate.
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PMID:Glutamine production by the isolated perfused rat heart during ammonium chloride perfusion. 24 May 5

Twelve infants with severe perinatal asphyxia were found to have elevated blood ammonia levels (302 to 960 microgram/100 ml). In the seven survivors, hyperammonemia was associated with CNS irritability, hyperthermia, hypertension, and wide neonatal heart rate oscillations. Follow-up examinations revealed severe neurologic dysfunction in five of seven infants. CNS depression, hyperthermia, hypertension, and a nonreactive, fixed heart rate characterized the infants that died. These findings suggest a clinical entity secondary to perinatal asphyxia whose signs and symptoms may be related to hyperammonemia.
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PMID:Hyperammonemia associated with perinatal asphyxia. 48 80

In two experiments with milk cows with permanent rumen fistula it was investigated whether, apart from urea being unpalatable, further physiologic parameters are responsible for the reduced feed intake. In experiment I the cows received 2, 3 resp 4% urea orally with barley coarse meal, or an equivalent amount was given continuously from the beginning of the feeding over a period of three hours through the fistula. When 2, 3 resp. 4% urea were given orally, the consumption went down in the first 30 min to 58, 52 resp. 40%. When urea was given rumenally, no depression of the consumption could be observed. There were distinct relations with the NH3-concentration in the rumen fluid. At 20 to 35 mg per 100 ml there was no resp. a slight depressioon only and at 40 mg a significant depression. When the concentration rose to greater than 50 mg, consumption was stopped. In experiment II the rumenal application of urea began two hours before the feeding. The high NH3-level shortly after the beginning of feeding (58 mg/100 ml) caused a stop in the feed consumption. No relation could be observed between the urea concentration in veinous blood and the feed intake.
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PMID:[Effective factors for the reduced feed intake of milk cows fed with rations containing urea]. 50 90

Secondary amines and amides of 5-aminoethyl-6-methoxyindan and 5-aminoethyl-6-methylindan were synthesized, and the blood pressure lowering effects and accompanying changes in heart rate were evaluated in the unanesthetized desoxycorticosterone acetate hypertensive rat. The acute toxicities of the compounds were determined in mice. The amines were significantly more potent than the amides as antihypertensive agents and also were more toxic. 5-(3,4-Dimethoxybenzyl)aminoethyl-6-methylindan produced the greatest depression in systolic blood pressure at the dose level studied. Structure-activity relationships relevant to blood pressure lowering, heart rate, and toxicity are discussed.
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PMID:Synthesis, toxicity, and cardiovascular properties of N-aralkyl- and N-acyl-5-aminoethylindans. 64 14

Pressure plethysmographic measurement of ventilation and electromyographic measurement of diaphragm activation in unanesthetized suckling opossums revealed spontaneous episodes of obstructive apnea. To better understand this phenomenon, intact animals were tested under different conditions of respiratory drive and during activation of pulmonary reflexes. Results showed that obstructed breaths were usually initiated with the lungs at or near the end-inspiratory level, and they occurred more frequently during air or oxygen breathing as compared with inhalation of hypercapnic or asphyxiant test gases. The latter two gas mixtures caused increases in ventilation; but depression of breathing resulting from pentobarbital anesthesia was not accompanied by obstructed breaths. It was initially considered that a reflex laryngeal response with changes in lung volume or lung irritation might trigger obstructive apnea; but pulmonary inflation and deflation as well as ammonia inhalation did not typically produce such an effect. The results indicate that mechanisms for obstructive apnea in the suckling opossum must account for the limited incidence of obstructed breaths during both ventilatory chemostimulation and anesthetic respiratory depression.
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PMID:An obstructive apnea in the suckling opossum. 70 85

Young male rats (100-130 g) were fed diets of equal energy content containing o.5, 1,2,3,5, and 18% lactalbumin consumed either freely or in restricted amounts. The rats receiving low protein diets failed to grow and mature. Those consuming the 0.5 and1% protein diets given freely developed the characteristic features of kwashiorkor including edema, while those receiving the diets in restricted amounts developed the characteristic features of marasmus. The rats fed low protein diets had low plasma levels of essential amino acids; however, the lysine level was well maintained. The plasma levels of nonessential amino acids, especially glycine, alanine, and aspartic and glutamic acids were raised in marasmic rats but were reduced in rats fed low protein diets ad libitum. Young and severly malnourished rats appeared to have limited ability to synthesize urea. Therefore, they excreted more ammonia and other nitrogenous substances such as ethanolamine, and when given an amino acid load, intermediary metabolites of the ingested amino acids. Rats fed low protein diets showed diminution of total liver DNA, RNA, and protein. In addition to the reduction of protein synthesis resulting from decreased cellular RNA, ribosomes from the livers of protein-deficient rats had reduced ability to synthesize proteins. This defect was associated with the detatchment of the ribosomes from endoplasmic reticulum membrane and the elevation of the proportion of monosomes to polyribosomes. Malnutrition did not produce any change in the turnover rate of liver RNA. Protein deficiency caused significant depression of serum insulin, thyroxine, and corticosterone levels. Theoverall conclusion is that mammalian metabolism is well adapted to dietary intake and that this adaptation is achieved through dietary control of synthesis and release of key metabolic hormones.
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PMID:Experimental protein and energy in the rat. 80 70

1. The use of Li pre-treatment in rats before high pressure oxygen exposure has been reported effective in controlling convulsions. This is an effect which is better demonstrated if exposure to oxygen follows shortly after Li injection than exposure following several hours later. 2. This study has investigated the hypothesis that the protective action of Li may be exerted, in the short term, by its removing ammonia from the blood and alleviating the latter's known toxic action. 3. A normal Li distribution time profile in unstressed rat brain and blood following intraperitoneal injection has been established. Brain and blood ammonia, amino acids and Li concentrations were also measured in Li-treated animals exposed and convulsed by oxygen. These measurements were made both shortly (15 min) and also several hours after (24 hr) Li treatment. Ammonia and amino acid values in Li-protected groups were compared to normal unstressed animal values and also to values in animals convulsed by oxygen unprotected by Li pre-treatment. 4. In rat brain abd blood significant (P less than 0-001) elevation of ammonia and glutamine and depression of gamma-amino butyric acid (brain only) and glutamate was noted following oxygen treatment in unprotected animals. Prior injection of Li 15 min before high pressure oxygen exposure delayed convulsions twice as long. Additionally if these animals were only exposed to oxygen for a period of time equal to that which would normally produce convulsions in unprotected animals, brain and blood ammonia and amino acids were maintained near to unstressed animal levels. Concomitantly, blood Li concentrations were considerably depressed below the values one would expect from the previously determined Li distribution time profile. 5. In rats exposed to high pressure oxygen 24 hr after Li treatment there was no protective action against high pressure oxygen convulsion, rather a potentiating effect for convulsion was seen. 6. These data present compelling evidence for the controlling effect of Li in rats, on rising blood ammonia concentration which occurs in high pressure oxygen exposure. The effect might well be due to the known chelating properties of Li with ammonia.
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PMID:Lithium protection against oxygen toxicity in rats: ammonia and amino acid metabolism. 97 69


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