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)

Hypotaurine increased in some tissues, especially in muscle, and urine of rats fed methionine excess diet. The significant depression of the body weight and food intake of rats caused by excess methionine was remarkably alleviated as previous reports and hypotaurine content in muscle and urine increased further by supplement with glycine to the excess methionine diet.
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PMID:Accumulation of hypotaurine in tissues and urine of rats fed an excess methionine diet. 162 89

Two trials were conducted to determine the utilization of manganese (Mn) as influenced by the level and source of Mn and the level of dietary calcium (Ca) in broiler chickens. Trial One was a 2 x 2 x 3 factorial arrangement of two Mn sources (Mn methionine or manganous oxide), two levels of dietary Ca (1.8 or 1.0), and three levels of supplemental Mn (30, 60, or 200 mg/kg) fed until 4 wk of age. Total phosphorus (available phosphorus) levels were 0.70% (0.48%) during all ages. High levels of dietary Ca caused a slower early rate of growth (0.53 vs. 0.64 kg) for chicks fed 1.8 vs 1.0% Ca, respectively. Chick weight was equivalent for all diets within the Ca-treatment group, except the dietary combination of high Ca and 200 mg/kg Mn as Mn methionine. Bone and liver Mn were significantly increased as the Mn level increased, but were not affected by the Mn source. Chicks fed 1.8% Ca had higher levels of bone Mn (9.28 ppm) than chicks fed 1.0% Ca (7.23 ppm). High levels of dietary Ca and 200 ppm Mn methionine dramatically depressed early growth, feed intake, and bone ash in this trial, raising the question of a diet x environment (heat-stress) effect. Trial Two was a 2 x 2 factorial arrangement of two levels of dietary Ca (1.8 or 1.0%) and two Mn sources (200 mg/kg Mn as Mn methionine or MnO) up to 3 wk of age in a controlled heat-stress environment. No growth depression in the chicks fed high levels of Ca and Mn methionine was observed. In the presence of high levels of dietary Ca, bone Mn was significantly higher when chicks were fed the MnO source. In summary, dietary Ca did not decrease Mn utilization in these trials, and availability of Mn in Mn methionine as a source compared to MnO depended on dietary Ca levels.
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PMID:Interaction of dietary calcium, manganese, and manganese source (Mn oxide or Mn methionine complex) on chick performance and manganese utilization. 172 5

Feeding a 13% CP diet based on corn and soybean meal and supplemented with methionine to laying hens results in reduced egg weight in comparison with hens fed a corn and soybean meal methionine-supplemented diet containing 16% CP. An experiment was conducted to determine whether the egg weight reduction could be eliminated by supplementing the low-protein diet with additional lysine, methionine, and tryptophan or by adding glycine and glutamic acid to increase the amino nitrogen to a level equivalent to 16% CP. The influence of the dietary treatments on the weight of the major egg components was also determined. In a second experiment, the influence of time of day of feeding the 13 or 16% CP diets on egg weight and egg components was determined. Adding additional amino nitrogen in the form of glycine and glutamic acid or increasing the levels of lysine, methionine, or tryptophan individually or in combination failed to prevent the depression in egg weight of hens fed the lower protein diet. Measurement of egg components demonstrated that the reduction in egg weight was primarily associated with a reduction in albumen content of the egg. Feeding a high-protein diet from 1400 to 0800 h and a low-protein diet from 0800 to 1400 h resulted in egg weight equivalent to that from hens continuously fed the high-protein diet. The lower weight of the albumen in eggs from hens fed a 13% CP diet may be due to a lower availability of amino acids for protein synthesis during the 3- to 4-h period when the ovum is in the magnum.
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PMID:Influence of protein concentration, amino acid supplementation, and daily time to access to high- or low-protein diets on egg weight and components in laying hens. 178 67

A 2-year-old girl with medulloblastoma who had postoperative radiotherapy and intrathecal administration of methotrexate is reported. Five months after radiation and chemotherapy, she developed involuntary movement. Positron emission tomography (PET) demonstrated that the metabolic rate of glucose was depressed markedly in the temporal and occipital lobes, indicative of metabolic depression induced by radiation. Prompt initiation of steroid therapy ameliorated the patient's neurological symptoms. Follow-up PET revealed an increase in 18F-fluorodeoxyglucose uptake in the entire brain, including temporal and occipital lesions. No areas with high accumulation of (11C-methyl)-L-methionine were detectable. We concluded that PET may be useful in establishing an early diagnosis of radiation injury of the brain and in monitoring metabolic changes following radiation in brain tumor patients.
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PMID:Demonstration of cerebral radiation injury with metabolic positron emission tomography images. 182 36

1. The synthetic Met-enkephalin, D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin (FK 33-824). 1 or 2 micrograms, after its injection into the nucleus tractus solitarius (NTS) of Wistar rats, anesthetized with pentobarbital and breathing spontaneously, produced a transient increase in blood pressure followed by sustained and significant (P less than 0.05) hypotension and bradycardia. This occurred in a dose dependent manner. 2. FK 33-824 in the NTS, 1 or 2 micrograms, also produced a marked respiratory depression. 3. In anesthetized rats, in which hypoventilation was prevented by mechanical ventilation, there was a definite reduction in blood pressure and heart rate that was considerably and significantly (P less than 0.05) less than that observed in spontaneously breathing rats. 4. Blood pressure fluctuations occurred after NTS injection that were more marked in spontaneously breathing animals but still occurred in animals that were ventilated mechanically. 5. FK 33-824, 1 and 2 micrograms in the NTS was fatal within 100 min for all animals but was prevented by mechanical ventilation. Higher doses of FK 33-824, 10 micrograms in the NTS, however, induced fatal ventricular arrhythmias even in the mechanically ventilated rat. 6. Thus, FK 33-824 in the NTS decreases blood pressure and heat rate in spontaneously breathing as well as mechanically ventilated rats, but much of the effect on blood pressure and heart rate is due to the profound respiratory depression in the spontaneously breathing rat.
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PMID:D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin in the nucleus tractus solitarius of the rat produces cardiorespiratory depression. 186 20

1. It has been established that chronic hyperammonaemia, whether caused by portacaval shunting or other means, leads to a variety of metabolic changes, including a depression in the cerebral metabolic rate of glucose (CMRGlc) increased permeability of the blood-brain barrier to neutral amino acids, and an increase in the brain content of aromatic amino acids. The preceding paper [Jessy, DeJoseph & Hawkins (1991) Biochem. J. 277, 693-696] showed that the depression in CMRGlc caused by hyperammonaemia correlated more closely with glutamine, a metabolite of ammonia, than with ammonia itself. This suggested that ammonia (NH3 and NH4+) was without effect. The present experiments address the question whether ammonia, in the absence of net glutamine synthesis, induces any of the metabolic symptoms of cerebral dysfunction associated with hyperammonaemia. 2. Small doses of methionine sulphoximine, an inhibitor of glutamine synthetase, were used to raise the plasma ammonia levels of normal rats without increasing the brain glutamine content. These hyperammonaemic rats, with plasma and brain ammonia levels equivalent to those known to depress brain function, behaved normally over 48 h. There was no depression of cerebral energy metabolism (i.e. the rate of glucose consumption). Contents of key intermediary metabolites and high-energy phosphates were normal. Neutral amino acid transport (tryptophan and leucine) and the brain contents of aromatic amino acids were unchanged. 3. The data suggest that ammonia is without effect at concentrations less than 1 mumol/ml if it is not converted into glutamine. The deleterious effect of chronic hyperammonaemia seems to begin with the synthesis of glutamine.
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PMID:Hyperammonaemia does not impair brain function in the absence of net glutamine synthesis. 187 6

Male rats were fed sulfur and nonsulfur amino acid-supplemented diets, and the response of cysteine sulfinic acid decarboxylase (CSAD) activity was determined. After adaptation to a casein-based basal diet, rats were fed diets containing additions of L-methionine. Hepatic CSAD activity decreased in a dose-dependent manner. Significant depression of CSAD activity in liver was evident within 24 h of feeding rats a methionine-supplemented diet. Depression of enzyme activity was reversed upon refeeding the basal diet. After rats were fed diets supplemented with methionine, cystine, homocystine, S-methyl-L-cysteine, phenylalanine, leucine, or ethionine for 14 days, hepatic CSAD activity in rats fed S-methyl-L-cysteine-, phenylalanine-, or leucine-supplemented diets was not depressed compared with activity in rats fed a basal diet. In contrast, CSAD activity in livers of rats fed cystine-, homocystine-, methionine-, or ethionine-supplemented diets was 60, 40, 40, and 8%, respectively, of the activity in livers from control rats. Immunochemical detection and quantification of CSAD protein in rat liver indicated that CSAD protein concentration was correlated to CSAD activity. CSAD activity may be specifically regulated by sulfur amino acids metabolized by the S-adenosylmethionine-dependent pathway of methionine metabolism.
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PMID:Dietary sulfur amino acid modulation of cysteine sulfinic acid decarboxylase. 195 78

The synthesis of the cytoskeletal protein actin exhibits, in the rat hypothalamus, a diurnal variation with maxima during morning hours. The objective of the present study was to assess whether melatonin injection could affect the in vitro incorporation of 35S-methionine into actin, as well as the levels of actin mRNA, in the hypothalamus of adult male rats treated either acutely or chronically with the hormone at 10:00 or 18:00. Injection of 100 micrograms/kg of melatonin for ten days at either time induced a significant depression in the incorporation of 35S-methionine into a 43 kDa protein with the electrophoretic mobility of actin. The specific activity of total soluble proteins after labeled methionine incubations decreased only after evening melatonin administration (100 micrograms/kg, ten days). Hypothalamic actin mRNA levels, quantitated by dot-blot analysis, decreased only after the injection of 100 micrograms/kg melatonin for ten days at 10:00. Neither a 10-micrograms/kg dose of melatonin, nor a single injection of 100 micrograms/kg melatonin, caused any significant change in the parameters examined. Melatonin (100 micrograms/kg for ten days) did not modify hypothalamic somatostatin or H-Ras mRNA concentration. These results suggest the existence of an inhibitory effect of melatonin on hypothalamic actin synthesis.
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PMID:Time-dependent effect of melatonin on actin mRNA levels and incorporation of 35S-methionine into actin and proteins by the rat hypothalamus. 197 1

A study was made of the blood and tissue oxygen regime in patients with vibratory disease (VD) induced by local vibration and of the importance of lipid peroxidation (LPO) in oxygenation disorders. Venous hyperoxia, a decrease of the arteriovenous difference according to oxygen, the percentage of oxygen utilization by tissues, shift of the acid-base balance towards metabolic acidosis were established, attesting to tissue hypoxia that increased with the gravity of VD. The importance of a steady activation of LPO and depression of the antioxidant system in the pathogenesis of hypoxia associated with VD was supported by the correlation analysis data on oxygen balance and LPO, the functional and metabolic characteristics of red blood cells (according to the viscosity of red blood cell suspension and the content in the cells of SH-groups, lipoproteins and histidine) and platelets (according to aggregation in response to ADP and thrombin) as well as by the level of blood serum fluorescence. The authors provide evidence for the use of antioxidants (a complex of alpha-tocopherol with ascorbic acid and methionine and calcium antagonists of the nifedipine group), giving a membranostabilizing effect, in multimodality treatment of patients afflicted with VD.
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PMID:[Cell-membrane aspects of the pathogenesis of hypoxia in vibration disease induced by local vibration]. 204 32

The purpose of this study was to investigate the effect of the synthetic Met-enkephalin, D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin (FK 33-824), on blood pressure, heart rate, respiratory rate and survival, after its injection into the 4th cerebral ventricle of Wistar rats. The animals were either anesthetized with pentobarbital and breathing spontaneously or unanesthetized. The unanesthetized rats were previously instrumented with cannulas in the 4th cerebral ventrical and a systemic artery. In anesthetized rats, intracerebroventricular administration of FK 33-824 produced a transient increase in blood pressure followed by sustained hypotension, bradycardia and respiratory depression in a dose-dependent manner. Fatalities were observed over a 150-min observation period and were a function of dose. Pretreatment with atropine sulfate (1 mg/kg i.v.) produced an accentuated response with greater hypotension, bradycardia and shorter survival. In another group of anesthetized rats, in which hypoventilation was prevented by mechanical ventilation, blood pressure and heart rate were not as reduced as in spontaneously breathing rats. Hypotension, bradycardia and hypoventilation were less marked in unanesthetized rats, compared to anesthetized rats. Thus, FK 33-824 in the 4th cerebral ventricle of the rat produces marked changes in blood pressure in anesthetized as well as unanesthetized animals, but these changes were less in the unanesthetized or mechanically ventilated animal and greater after atropine, suggesting that these effects are mediated by respiratory depression and are antagonized by the cholinergic nervous system.
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PMID:Cardiorespiratory responses to D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin after administration into the fourth cerebral ventricle of the rat: interaction with cholinergic mechanisms. 206 74


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