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)

Reports concerning the interaction between steroidal contraceptives (the combined pill) and vitamins indicate that in users the mean serum-vitamin-A level is raised and the mean serum-vitamin-B2 (riboflavine), vitamin-B6 (pyridoxine), vitamine-C, folic-acid, and vitamin-B12 levels are reduced. Other vitamins have been insufficiently studied for comment. Biochemical evidence of co-enzyme deficiency has been reported for vitamin B2, vitamin B6, and folic acid. Clinical effects due to vitamin deficiency have been described for vitamin B6--namely, depression and impaired glucose tolerance. Folic-acid deficiency with megaloblastic anaemia has been reported in only 21 cases.
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PMID:Vitamins and oral contraceptive use. 4 28

Bone marrow fragments from 10 patients with a megaloblastic anaemia due to vitamin B12 or folate deficiency were studied by electron microscopy and electron microscope autoradiography. A proportion of the erythroblasts showed ultrastructural abnormalities. Some of the cells containing autophagic vacuoles, large siderosomes, iron-laden mitochondria, irregularly shaped nuclei, membrane-bound nuclear clefts, or incomplete nuclear membranes were found to be capable of DNA, RNA and protein synthesis. Other cells showed advanced degenerative changes such as the distension of the perinuclear space, the clumping of cytoplasmic organelles near the nucleus and a reduction in the electron density and ribosome content of the cytoplasm. Most of these grossly abnormal cells suffered from either a marked depression or an arrest in protein and RNA synthesis, and were presumably destined for phagocytosis by reticulum cells.
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PMID:Electron microscope and high resolution autoradiographic studies of megaloblastic erythropoiesis. 40 60

Preoperative folate levels were initially normal in 30 patients with gastrointestinal tract disease but fell within 48 h by 60-95% in 20 patients who received intravenous nutrition for 6-12 d with aminoacid-sorbitol-ethanol (ASE). This depression persisted in patients not given folate supplements. Folate levels in 10 control patients not given ASE showed only minimal decline. Haematological changes were reduced to a minimum in 10 patients given 0.5 mg i.v. folic acid daily whilst eight unsupplemented patients showed evidence of megaloblastic haemopoiesis. Three of these eight patients developed thrombocytopenia and/or leukopenia which was fatal in one patient.
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PMID:Acute folate deficiency associated with intravenous nutrition with aminoacid-sorbitol-ethanol: prophylaxis with intravenous folic acid. 41 77

Rates of glucose, glycine, and folic (pteroylglutamic) acid absorption were determined for a 30 cm jejunal segment in vivo, with a double-lumen tube perfusion system, in 10 Zambian African women with a mean haemoglobin concentration of 5-1 (3-5-9-2) g/dl. In four the anaemia was megaloblastic (due to folate deficiency) and in six hypochromic. Perfusion solutions contained (1) glucose 200 mmol/1, (2) glycine 100 mmol/1, and (3) folic acid 250 mug/1. D-xylose absorption after a 25 g oral load was determined in them, and also in 18 additional patients (11 had megaloblastic and seven either hypochromic or haemolytic anaemia). Xylose absorption tests were significantly impaired in the patients with megaloblastic compared with hypochromic or haemolytic anaemia (P less than 0-001); those with untreated megaloblastic anaemia had a greater abnormality than those who had started treatment. Mean glucose, glycine, and folic acid absorption rates were similar to those in controls, and the rates in patients with megaloblastic and hypochromic anaemia were not significantly different. Correlation between glucose absorption rate and xylose excretion was, however, significantly (P less than 0-02). If more patients had been studied it seems likely therefore that a significant impairment of glucose absorption rate in the presence of megaloblastic anaemia would also have been demonstrated. In this investigation anaemia per se did not affect glucose, glycine, or folic acid absorption rates or xylose absorption, but xylose absorption was reduced in patients with megaloblastic anaemia. That abnormality was probably related to folate deficiency, and the underlying mechanism seems to be different from that causing impairment of monosaccharide absorption in patients with systemic bacterial infections. Mean glycine and folic acid absorption rates were not altered by megaloblastic anaemia, indicating that folate deficiency does not cause a general depression of absorption.
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PMID:Absorption of xylose, glucose, glycine, and folic (pteroylglutamic) acid in Zambian Africans with anaemia. 97 99

Folate metabolism was studied in normal, folate-deficient and alcoholic man by tracer measurements of plasma clearance, urinary excretion, tissue storage and release of folate using both [3H]pteroylglutamic acid (3H-PteGlu) and 14C-methyl-H4PteGlu. Alcohol ingestion did not adversely affect tissue uptake of folates. Whether in normal or folate deficient subjects, the relative clearance rates of 3H-PteGlu and 14C-methyl-H4PteGlu were maintained in the face of alcohol ingestion and there was no evidence of increased urinary loss of intact vitamin or labelled breakdown products. As measured by the flushing technique, the rate of storage or tissue binding of 3H-PteGlu was not influenced by folate deficiency, folate store depletion or alcohol ingestion. However, alcohol may retard the release of methyl-H4PteGlu from tissue stores to plasma. A significantly greater recovery of 14C-methyl-H4PteGly with flush was observed in those normal subjects who ingested alcohol for 6 d. A partial block in the rate of release of tissue folate stores would be a possible mechanism behind the rapid depression in serum methyl-H4PteGlu levels and early induction of megaloblastic erythropoiesis which has been observed following acute alcohol ingestion.
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PMID:Folic acid metabolism in normal, folate deficient and alcoholic man. 99 Jan 85

Cell-mediated immunity has been studied in patients with 1) megaloblastic anemia of folic acid deficiency, 2)megaloblastic anemia of pregnancy, or 3) iron-deficiency anemia. Using dinitrochlorobenzene skin tests, phytohemagglutinin-stimulated lymphocyte transformation, and rosette inhibition by antilymphocyte globulin, we have shown that cell-mediated immunity is depressed in megaloblastic anemia due to folate deficiency; this depression was reversed by folate treatment. Cell-mediated immunity was not impaired by iron-deficiency anemia. Suggested interactions between iron deficiency and folate metabolism were not clarified by these studies.
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PMID:Depressed cell-mediated immunity in megaloblastic anemia due to folic acid deficiency. 111 20

Embryos of different ages from 24th to 120th hour of incubation were irradiated with a dose of 700 R gamma rays at a rate of 50 R/min. After irradiation peripheral blood was taken every 24 hours in order to control proliferation dynamics of megaloblastic and normoblastic cells. The results have shown that the cells of megaloblastic strain reduce much more the mitotic activity that those of normoblastic line. Although the cells of both strains after irradiation show depression in the proliferative activity, in transfer to polychromatophilic forms, megaloblasts disappear almost completely until normoblasts recover spontaneously. The nature of different radiosensitivity in these cell strains has been discussed.
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PMID:Different radiosensitivity of hematopoietic cells in chick-embryos. 116 77

The meaning of a low serum cobalamin level when the classic findings of pernicious anemia are lacking is undergoing reevaluation. We therefore studied the neurologic status of 11 patients who had low cobalamin levels without definite hematologic evidence of deficiency. Neurologic evaluation included pattern-shift visual and median and posterior tibial nerve somatosensory evoked potentials. None of the patients had megaloblastic changes in the blood or bone marrow, although 7 of the 11 had subtle cellular cobalamin disturbances demonstrated by an abnormal deoxyuridine suppression test result. Seven patients had normal Schilling test results and 2 had borderline results; however, 2 of the 5 patients tested further had food-cobalamin malabsorption, while a third had prepernicious anemia. The patients displayed a variety of neurologic problems, including dementia, depression, myelopathy, neuropathy, and seizure disorder; 1 patient was neurologically normal by clinical criteria. Evoked potential abnormalities were demonstrable in 8 of the 9 patients with subtle cobalamin deficiency, and in at least 5 cases the disturbance was central. In contrast, both patients whose low serum cobalamin levels were found on evaluation to be spurious had normal evoked potentials. Evoked potential abnormalities improved in the one patient retested after cobalamin therapy. These findings demonstrate that neurologic deficits occur not only in classic cobalamin deficiency but also in subtle or atypical cobalamin deficiency states in which anemia is absent and Schilling test results are normal. Electrophysiologic evidence of neurologic impairment is often present, even in patients without obvious clinical neurologic abnormalities.
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PMID:Neurologic and evoked potential abnormalities in subtle cobalamin deficiency states, including deficiency without anemia and with normal absorption of free cobalamin. 239 29

We report a case of methionine synthase deficiency associated with cellular immune deficiency discovered in a 14-year-old boy. Principal findings were: developmental delay, recurrent upper and lower respiratory tract infections, megaloblastic anemia, discovered at 3 months of age, unresponsive to cyanocobalamin and poorly responsive to folinic acid. Biochemical studies showed: an abnormal deoxyuridine suppression test despite normal serum folate, cobalamin and transcobalamin levels; a normal intracellular uptake of these two coenzymes; and an absolute requirement of methionine for fibroblast growth, suggestive of defective methionine synthesis. An absence of methionine synthase activity in the patient's bone marrow and a profound depression of this activity in lymphocytes and liver were found. Hypergammaglobulinemia with variable lymphopenia, depressed lymphocyte transformation after lectin or recall-antigen stimulation, defective delayed-type hypersensitivity and decreased natural killer activity were noted as well. The patient died at the age of 14.
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PMID:Megaloblastic anemia and immune abnormalities in a patient with methionine synthase deficiency. 342 20

The activity of the two folate dependent enzymes supplying carbon 2 and carbon 8 of the purine nucleus was assayed in the bone marrow of rats and man, as well as in rat livers. The activity of both enzymes was several fold greater in marrow than in liver. Inactivation of cobalamin by exposure to nitrous oxide did not affect the enzymes in rat marrow cells, although an appreciable effect on hepatic enzymes was found. The depression of hepatic glycinamide ribotide (GAR) transformylase in rats exposed to nitrous oxide was prevented by supplying a formate precursor, methylthioadenosine. There was a considerable rise in the activity of GAR transformylase in human marrow cells from patients with megaloblastic anaemia due to cobalamin deficiency but no change in activity in marrow from patients deficient in folate.
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PMID:Role of folate dependent transformylases in synthesis of purine in bone marrow of man and in bone marrow and liver of rats. 407 17


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