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)

Major depression is a serious disease with various systemic effects, including dysfunction of the immune response. Taurine has been known to be related to certain modifications of the immune system. The aim of this study was to determine the taurine concentration in lymphocytes of patients with major depression and to evaluate the influence of the antidepressant treatment with mirtazapine for six weeks on the levels of taurine. Gamma-aminobutyric acid, aspartate, glutamate and glutamine were also determined. Taurine, aspartate and glutamine levels were increased in the lymphocytes of depressed patients before mirtazapine treatment compared to the control group, and were normalized after treatment. Gamma-aminobutyric acid and glutamate did not differ between patients and controls. There was a significant and positive correlation between the severity of the disorder, measured by the Hamilton Rating Scale, and the concentration of taurine in the lymphocytes of depressed patients before treatment. This correlation was not observed after treatment and neither was there a correlation observed for the other amino acids. The present observations could be an indication of the relevance of taurine as a protective agent in the lymphocytes of patients with severe depression, and could be the result of modifications of taurine transport or efflux processes.
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PMID:Taurine concentration in human blood peripheral lymphocytes: major depression and treatment with the antidepressant mirtazapine. 1290 14

Strenuous bouts of prolonged exercise and heavy training are associated with depressed immune cell function. Furthermore, inadequate or inappropriate nutrition can compound the negative influence of heavy exertion on immunocompetence. Dietary deficiencies of protein and specific micronutrients have long been associated with immune dysfunction. An adequate intake of iron, zinc and vitamins A, E, B6 and B12 is particularly important for the maintenance of immune function, but excess intakes of some micronutrients can also impair immune function and have other adverse effects on health. Immune system depression has also been associated with an excess intake of fat. To maintain immune function, athletes should eat a well-balanced diet sufficient to meet their energy requirements. An athlete exercising in a carbohydrate-depleted state experiences larger increases in circulating stress hormones and a greater perturbation of several immune function indices. Conversely, consuming 30-60 g carbohydrate x h(-1) during sustained intensive exercise attenuates rises in stress hormones such as cortisol and appears to limit the degree of exercise-induced immune depression. Convincing evidence that so-called 'immune-boosting' supplements, including high doses of antioxidant vitamins, glutamine, zinc, probiotics and Echinacea, prevent exercise-induced immune impairment is currently lacking.
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PMID:Exercise, nutrition and immune function. 1497 37

HIV-1 encodes for one of the human glutathione peroxidases. As a consequence, as it is replicated, its genetic needs cause it to deprive HIV-1 seropositive individuals not only of glutathione peroxidase, but also of the four basic components of this selenoenzyme, namely selenium, cysteine, glutamine, and tryptophan. Eventually this depletion process causes severe deficiencies of all these substances. These, in turn, are responsible for the major symptoms of AIDS which include immune system collapse, greater susceptibility to cancer and myocardial infarction, muscle wasting, depression, diarrhea, psychosis and dementia. As the immune system fails, associated pathogenic cofactors become responsible for a variety of their own unique symptoms. Any treatment for HIV/AIDS must, therefore, include normalization of body levels of glutathione, glutathione peroxidase, selenium, cysteine, glutamine, and tryptophan. Although various clinical trials have improved the health of AIDS patients by correcting one or more of these nutritional deficiencies, they have not, until the present, been addressed together. Physicians involved in a selenium and amino-acid field trial in Botswana, however, are reporting that this nutritional protocol reverses AIDS in 99% of patients receiving it, usually within three weeks.
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PMID:How HIV-1 causes AIDS: implications for prevention and treatment. 1505 Jan 5

In experiments on 182 white male rats hepatitis was modelled by percutaneous injection of 0.1 ml/500 g of tetrachloromethane (TCM) dissolved in olive oil. TCM was injected every other day for 65 days. After development of hepatitis (in 65 days) synthesis of glutamine and urea, partial oxygen pressure in the liver were studied. It is shown that modelling of chronic hepatitis leads to impairment of glutamine and urea synthesis, reduction of tissue blood flow and oxygen partial pressure. It is suggested that the reason of these changes is inhibition activity of glutamate dehydrogenase, arginase and short-term depression activity of phosphate-dependent glutaminase. The changes in the enzymatic activity lead to lowering tissue level of glutamine, urea, accumulation of ammonia ions. These changes persist for 14 days after the last injection of tetrachloromethane.
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PMID:[The ammonia neutralization function of the liver in chronic active hepatitis]. 1505 75

The early detection and appropriate treatment of brain ischemia is of paramount importance. The interstitial concentrations of neurotransmitter amino acids are often used as an index of neuronal injury. However, monitoring of non-neurotransmitter amino acids may be equally important. We have studied the behavior of 10 amino acids during K(+)-induced spreading depression (application of 70 mM KCl during 40 min) and global forebrain ischemia (two-vessel occlusion with hypotension during 20 min). The concentrations of glutamate, aspartate, taurine, GABA, glycine, and alanine, measured in the rat striatum by microdialysis, increased during both ischemia and spreading depression, whereas glutamine concentrations decreased in both cases. Only ischemia, but not spreading depression, led to enhanced release of serine, threonine, and asparagine. We thus conclude that an elevation in the interstitial concentrations of non-neurotransmitter amino acids is specific to deep ischemic injury to nervous tissue. We propose the monitoring of serine, asparagine, and threonine, together with excitatory amino acids, as an index of the degree of ischemic brain injury.
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PMID:Interstitial concentrations of amino acids in the rat striatum during global forebrain ischemia and potassium-evoked spreading depression. 1526 Jan 29

Immune-enhancing diets contain nutrients that have putative benefits, including arginine, (n-3) fats, glutamine, nucleotides, and structured lipids. Although under most circumstances the systemic inflammatory response is beneficial to the host, improving the eventual outcome of injury, infection, or inflammation, excessive proinflammation (leading to cardiac, hepatic, and mitochondrial dysfunction) or excessive counterinflammation (leading to immune depression) can worsen outcome. In critically ill septic patients, the synthesis of arginine can be exceeded by its catabolism to nitric oxide (NO) and urea, rendering arginine conditionally essential. In patients with sepsis, increased production of NO increases serum nitrite and nitrate levels, whereas levels in patients with trauma and trauma with sepsis are lower than in controls. In septic patients, supplemental arginine might further increase NO levels and be potentially harmful through excessive proinflammation. However, administration of increased amounts of arginine might improve immune function in surgical and trauma patients by increasing NO production in macrophages. When the diet provides at least 1 g of the (n-3) fatty acids eicosapentaenoic and docosahexaenoic acid combined, 2-series eicosanoids (prostaglandins, prostacyclins, thromboxanes) are replaced partially by 3-series eicosanoids, and 4-series leukotrienes are replaced partially by 5-series leukotrienes that are less proinflammatory. Thus, the effects of arginine and (n-3)-fat supplementation might be expected to be complementary-arginine might improve cytokine and NO production in patients with immunodepression, whereas (n-3) fats might be beneficial when there is excessive proinflammation, particularly when supplemental arginine is supplied, by reducing cytokine-induced eicosanoid production.
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PMID:Practical recommendations for immune-enhancing diets. 1546 3

Forty weaned barrows (5.32 +/- 0.3 kg BW) at 17 +/- 2 d of age were used to investigate the effects of feeding glutamine and spray-dried plasma on the growth performance, small intestinal morphology, and immune responses of Escherichia coli K88-challenged pigs. Pigs were allotted to four treatments including: 1) nonchallenged control (NONC); 2) challenged control (CHAC); 3) 7% (as-fed basis) spray-dried plasma (SDP); and 4) 2% (as-fed basis) glutamine (GLN). On d 11 after weaning, all pigs were fitted with an indwelling jugular catheter. On d 12 after weaning, pigs in the CHAC, SDP, and GLN groups were orally challenged with skim milk E. coli K88 culture, whereas pigs in the NONC group were orally inoculated with sterilized skim milk. Rectal temperatures and fecal diarrheic scores were recorded and blood samples collected at 0 (baseline), 6, 12, 24, 36, and 48 h after the challenge for serum hormone and cytokine measurements. At 48 h postchallenge, all pigs were killed for evaluation of small intestinal morphology. There was no effect of feeding SDP or GLN on growth performance during the 11-d prechallenge period (P = 0.13). At 48 h after the challenge, CHAC pigs had decreased ADG (P = 0.08) and G:F (P = 0.07) compared with the NONC pigs; however, SDP and NONC pigs did not differ in G:F, and GLN and NONC pigs did not differ for ADG and G:F. At 6, 36, and 48 h after the challenge, CHAC, SDP, and GLN pigs had increased rectal temperature relative to the baseline (P = 0.09). At 12 and 36 h after the challenge, CHAC pigs had the highest incidence of diarrhea among treatments (P = 0.08). Serum IL-6 and ACTH were not affected by treatment or time after E. coli challenge (P = 0.11). In proximal, midjejunum, and ileum, CHAC pigs had greater villous atrophy and intestinal morphology disruption than NONC pigs (P < 0.01), whereas SDP and GLN pigs had mitigated villous atrophy and intestinal morphology impairment after E. coli challenge. Pigs in the SDP had the lowest GH at 12 h and the greatest GH at 36 h after the challenge among treatments (P = 0.08). Pigs in the NONC had the highest IGF-1 at 12 and 36 h postchallenge (P < 0.04). These results indicate that feeding glutamine has beneficial effects in alleviating growth depression of E. coli K88-challenged pigs, mainly via maintaining intestinal morphology and function, and/or possibly via modulating the somatotrophic axis.
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PMID:Effect of glutamine and spray-dried plasma on growth performance, small intestinal morphology, and immune responses of Escherichia coli K88+-challenged weaned pigs. 1570 60

Glycyl-glutamine (Gly-Gln; beta-endorphin(30-31)) is an endogenous dipeptide synthesized from beta-endorphin(1-31). Previous investigations have shown that Gly-Gln inhibits the cardiovascular and respiratory depression caused by morphine and beta-endorphin(1-31), but it does not interfere with opioid analgesia. In this study, we tested whether Gly-Gln administration would influence morphine-induced conditioned place preference, tolerance, dependence, or withdrawal. For place preference experiments, rats were conditioned with morphine sulfate (2.5 mg/kg i.p.) or saline on alternate days for 6 days and tested on day 7. Glycyl-glutamine (1-100 nmol i.c.v.) pretreatment inhibited acquisition of a conditioned place preference to morphine significantly. Glycyl-glutamine (100 nmol i.c.v.) also blocked expression of a pre-established morphine place preference, but it did not interfere with acquisition of a conditioned place preference to palatable food, and it did not produce place preference or aversion when given alone to morphine-naive animals. To induce antinociceptive tolerance, rats were treated with morphine (10 mg/kg i.p.) twice daily for 7 days, and morphine antinociception was evaluated with the tail-flick test. Glycyl-glutamine (100 nmol i.c.v.) pretreatment delayed the onset of morphine tolerance significantly and partially reversed pre-established tolerance. Morphine dependence and withdrawal were assessed by measuring naloxone-precipitated withdrawal symptoms. Glycyl-glutamine inhibited the development of morphine dependence when given to rats twice daily immediately before they received morphine (10 mg/kg i.p.) and suppressed withdrawal symptoms of rats with subcutaneously implanted morphine pellets when administered 5 min before withdrawal was induced with naloxone. Glycyl-glutamine thus attenuates morphine-induced conditioned place preference, tolerance, dependence, and withdrawal without compromising morphine analgesia.
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PMID:Glycyl-glutamine, an endogenous beta-endorphin-derived peptide, inhibits morphine-induced conditioned place preference, tolerance, dependence, and withdrawal. 1607 99

Converging evidence has indicated that hyperglutamatergic activity and GABAergic dysfunction may play important roles in the neurobiology and treatment of depression and other mood disorders. In this study, in vivo 1H[13C] magnetic resonance spectroscopy was used to quantify the effects of acute phenelzine administration on cortical energetics, glutamate neurotransmission, and GABA synthesis flux. The time-resolved kinetics of cortical [4-13C]glutamate, [4-13C]glutamine, and [2-13C]GABA turnover from i.v.-infused [1,6-13C2]glucose was measured at 11.7 T in alpha-chloralose anesthetized rats four hours after phenelzine treatment (10 mg/kg, i.p.) and in non-treated controls. The rate of the tricarboxylic acid cycle flux was not affected by phenelzine treatment compared with the non-treated group (0.46+/-0.05 vs. 0.50+/-0.05 micromol/g/min, respectively). The rate of the glutamate-glutamine cycling flux between neurons and glia in the phenelzine-treated group was significantly reduced (from 0.16+/-0.04 to 0.10+/-0.03 micromol/g/min), providing in vivo evidence that phenelzine attenuates glutamate neurotransmission. Following phenelzine treatment, the cortical GABA concentration increased significantly (from 1.02+/-0.17 to 2.30+/-0.26 micromol/g), while the GABA synthesis flux was unchanged (from 0.07+/-0.02 to 0.06+/-0.02 micromol/g/min). The possible role of augmented GABAergic function resulting from elevated GABA levels in the observed modulatory effect of phenelzine on the glutamate-glutamine cycling flux was discussed. The reduced glutamate-glutamine cycling flux observed in this study suggests that, in addition to its effects on monoaminergic and GABAergic systems, the attenuation of glutamate neurotransmission resulting from phenelzine administration may also contribute to its efficacy in the treatment of depression. This study is the first demonstration that the glutamate-glutamine cycling flux, which can be measured non-invasively in the human brain in vivo, was altered due to the action of a psychotropic drug.
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PMID:In vivo evidence for reduced cortical glutamate-glutamine cycling in rats treated with the antidepressant/antipanic drug phenelzine. 1615 87

Abnormalities in L-glutamic acid (glutamate) and GABA signal transmission have been postulated to play a role in depression, but little is known about the underlying molecular determinants and neural mechanisms. Microarray analysis of specific areas of cerebral cortex from individuals who had suffered from major depressive disorder demonstrated significant down-regulation of SLC1A2 and SLC1A3, two key members of the glutamate/neutral amino acid transporter protein family, SLC1. Similarly, expression of L-glutamate-ammonia ligase, the enzyme that converts glutamate to nontoxic glutamine was significantly decreased. Together, these changes could elevate levels of extracellular glutamate considerably, which is potentially neurotoxic and can affect the efficiency of glutamate signaling. The astroglial distribution of the two glutamate transporters and L-glutamate-ammonia ligase strongly links glia to the pathophysiology of depression and challenges the conventional notion that depression is solely a neuronal disorder. The same cortical areas displayed concomitant up-regulation of several glutamate and GABA(A) receptor subunits, of which GABA(A)alpha1 and GABA(A)beta3 showed selectivity for individuals who had died by suicide, indicating their potential utility as biomarkers of suicidality. These findings point to previously undiscovered molecular underpinnings of the pathophysiology of major depression and offer potentially new pharmacological targets for treating depression.
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PMID:Altered cortical glutamatergic and GABAergic signal transmission with glial involvement in depression. 1623 Jun 5


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