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)

Tranylcypromine produces behavioral excitation while pargyline produces depression. Tranylcypromine increased brain tryptophan which led to an accumulation of tryptamine. The levels of tryptamine after tranylcypromine were found to be 3 times those found after pargyline.
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PMID:Effects of tranylcypromine and pargyline on brain tryptamine. 87 Mar 36

The study dealt with the level of and diurnal alterations in the concentration of tryptophan, free tryptophan and tyrosine in the blood plasma of 20 inhibited depression patients and 10 healthy controls. The results suggested that there was no distinct relationship between either the total plasma tryptophan or plasma tyrosine level and depression. On the other hand, the free plasma tryptophan level was, at all the times of day at which measurements were made, either significantly or almost significantly higher in the patients than in the controls. It was further found that the results of measurement were related to the patients' clinical improvement, as measured by the Hamilton test, in such a way that after four weeks of treatment the free plasma tryptophan level in 'poorly improved' patients continued to be significantly higher in comparison with the controls, whereas the values for the 'well improved' patient group did not differ greatly from the corresponding values for the control group any longer. It may be hypothesized that the rise in the free plasma tryptophan in depressive patients might represent an effort made by the peripheral body to compensate for the slowed-up serotonin metabolism of the brain, whereby the tryptophan mobilized from the periphery would serve as a sort of 'endogenous antidepressant' provided by the organism itself.
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PMID:The daily rhythm of plasma tryptophan and tyrosine in depression. 94 98

Exposure of dilute aqueous solutions of tryptophan to near UV light (320 to 390 nm) at subsolar levels yields fluorescent photoproducts capable of inhibiting the growth and differentiation of cultured mouse embryonic fibroblasts and fertilized sea urchin eggs. The ability of these cells to incorporate labelled precursors of protein, RNA, and DNA into their respective macromolecules was markedly inhibited by adding tryptophan preirradiated with near UV light to their incubation media. Thus the inhibition of growth and differentiation of these cells seems to result from a depression of their ability to synthesize macromolecules in the presence of the photoproducts.
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PMID:Inhibition of cell growth by near ultraviolet light photoproducts of tryptophan. 94 71

By treating rats with lithium chloride or cocaine hydrochloride, or lithium chloride followed by cocaine hydrochloride, we have shown the antagonistic effects of these drugs on two mechanisms that may be involved in regulating serotonin 5-HT) synthesis in the striate cortex. Lithium chloride (5 to 10 meq/kg/day) stimulates the relative velocity of the active uptake of labelled tryptophan and proportionally enhances the conversion of labelled tryptophan to 5-HT in synaptosomally enriched preparations. With continued administration of lithium chloride, the activity of tryptophan hydroxylase from the median raphe and subsequently in lysed synaptosomal preparations from striate cortex is reduced; the substrate uptake remains enhanced, but the conversion of substrate to transmitter returns to control levels. In contrast, an injection of cocaine hydrochloride inhibits the high affinity uptake of tryptophan, reducing the conversion of the amino acid to 5-HT and resulting in an increase in the biosynthetic enzyme activity. However, administration of cocaine hydrochter three daily lithium chloride injections (10 meq/kg) results in no apparent effects on substrate uptake, conversion, or enzyme activity. We theorize that the effect of lithium was to push two regulatory parameters (the uptake of substrate and the enzyme activity) to their respective functional upper and lower limits, leaving the serotonergic neurons "buffered" against the "usual" effects of the stimulant drug, and offer this neurobiological model for consideration in relation to the clinical effects of lithium in the prophylaxis of both mania and depression in some patients.
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PMID:A neurobiological model for the symmetrical prophylactic action of lithium in bipolar affective disorder. 98 97

The Authors describe the various anomalies of the metabolism of tryptophan that are observed in various diseases. The oxidative pathway is most important of the metabolic pathway of the amino acid; the degredation of tryptophan is particularly influenced by steroid hormones and vitamins' want. The metabolic anomalies are demonstrable both in malignant tumors (mostly in bladder cancer and Hodgkin's disease), both during psychiatric diseases (such as depression and schizophrenia) and in the diseases of connective tissue in addition to congenital errors of the degradation of tryptophan (such as Hartnup's disease, tryptophanuria and 3-hydroxychinureninuria). The metabolic pictures are manifest after amino acid's in the diseases of connective tissue but are independent for clinical seriousness and, in any case, less significant than those observed in other pathological pictures, mostly in Hodgkin's disease. The existence of anomalies of tryptophan's metabolism is certainly shown in many diseases, however the true physiopathogenetic meaning of these metabolic alterations is not yet specified. Particularly it is not definite if these alterations are the cause of diseases, which they appear in, or if they are secondary alterations.
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PMID:[Clinical significance of changes in tryptophan metabolism]. 109 26

A summary of the effects of contraceptive pills on vitamins in the b lood is presented. The significant increase of Vitamin-A in the plasma of contraceptive users is believed to be a result of the increase of bet alipoprotein, which binds chiefly to Vitamin-A. Although high concentrations of Vitamin-A have caused teratogenicity in test animals, the increase found in humans using contraceptive pills is not high enough to cause risk. A lowering of Vitamin-B6 (pyridoxin) levels has occurred with the use of contraceptive pills. This can cause alteration in the metabolism of tryptophan, which could cause depression in pill users. The lack of pyridoxine can also increase the production of xanthuric acid which binds with insulin, resulting in a decreased glucose tolerance. A decrease in folic acid in pill users has also been observed, caused by some effect of the pill on the folate deconjugate. The Vitamin-B12 level is also lowered for unascertainable reasons related to the decrease in folic acid. No anemia occurs in spite of the lowered Vitamin-B complex levels in the blood. A lack in Vitamin-C in users of pills containing estrogens is possibly effected by a corresponding increase between estrogens and ceruloplasmin, a protein active in the oxidation of ascorbic acid. This lack of Vitamin-C has had no clinical significance thus far.
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PMID:[P-pills and vitamins]. 114 66

This letter is a response to an article describing the efficacy of administering large doses of tryptophan to depressive patients taking oral contraceptives. This letter-writer argues that the salient action of mood elevation is a result of the supplemental pyridoxine (vitamin B) which ameliorates the deficiency induced by oral contraceptive use that leads to depression resulting from inhibition of synthesis of biogenic amines in the central nervous system. Instead of large doses of tryptophan, which may cause dangerous accumulations of possibly carcinogenic and diabetogenic metabolites when therapy for depression is indicated, pyridoxine should be administered together with the tryptophan; the tryptophan should be discontinued once the deficiency is corrected, although the vitamin therapy should continue throughout oral contraceptive use.
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PMID:Letter: supplementary pyridoxine given to women using oral contraceptives. 115 24

Plasma albumin levels were measured in partially hepatectomized, sham operated and control rats. The levels fell in both the partially hepatectomized and sham operated groups; while the latter group returned to normal within a few days, the low plasma albumin in the partially hepatectomized animals was sustained. Albumin synthesis rates in the isolated perfused rat liver were measured in the three groups of animals at varying intervals after partial hepatectomy. There was a significant depression of albumin synthesis rate in terms of both liver and whole animal weights when compared to the sham operated and control animals. This depression was almost completely reversed by the addition of arginine, asparagine, isoleucine, leucine, lysine, methionine, phenylalanine, proline, threonine, tryptophan and valine added together to 10 times their normal plasma concentrations. The addition of hydrocortisone had no effect on the albumin synthesis rate after partial hepatectomy. Studies in vivo in the three groups of animals (partially hepatectomized, sham operated and control animals) revealed a fall in the albumin catabolic rate after partial hepatectomy coinciding with the fall in the albumin synthesis rate. An hypothesis whereby the amino acids may have their stimulatory effect is proposed.
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PMID:Albumin synthesis and catabolism following partial hepatectomy in the rat. The effects of amino acids and adrenocortical steroids on albumin synthesis after partial hepatectomy. 115 98

(1) Height, weight, total body potassium, exchangeable sodium, bromide space, total body water and concentrations of sodium, potassium and chloride in plasma were measured in control subjects and individuals suffering from alcoholism, with techniques which included body counting and a multiple isotope method using 24Na, 82Br and 3H2O. (2) No differences were found between control and alcoholic subjects so there was no evidence that chronic alcoholism altered body composition. In particular there was no eficence of cellular damage or loss which would have been reflected in changes in KT or KIN. (3) The data were combined and were analysed to give information on the relationships of the variates. (4) On-going work by the author on tryptophan metabolism in primary alcoholics is compared to Shaw's findings on the kinetic behaviour of tryptophan in affective disorder. The possible prophylactic value of L-tryptophan (Optimax) in preventing both recurrent depression and recurrent alcohol abuse is outlined. (5) Data on body composition in normal subjects not hitherto available in the literature is provided.
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PMID:Body composition in control, alcoholic and depressive individuals using a multiple isotope technique and whole body counting of potassium. 118 Jan 50

Biochemical human post-mortem studies on depressed patients indicate an unspecific deficiency of neurotransmitters in several brain areas. The loss of drive of these patients could be correlated with a decrease of striatal dopamine concentration. Noradrenaline was significantly diminished in red nucleus, a fact which points to the characteristic posture of depressed patients. Serotonin was diminished in all brain areas. During remission all values trended to be normal. There also exists a circadian disrhythm in depressed patients resulting in lowered VMA- and HVA-levels in urines during the morning and a remission to normal values in the evening. This agrees with the findings of lowered blood tyrosine levels in the morning. The ratio of blood tyrosine and tryptophan is disturbed during depression and recovers during remission. Central and peripheral biochemical mechanisms seems to be involved in depression syndrom.
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PMID:Biochemical post-mortem findings in depressed patients. 118 63


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