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)

The biological mechanisms through which oral contraceptives influence the central nervous system and produce depression were examined. Oral contraceptives reduce the level of serotonin and norepinephrine available at the central adrenergic receptor sites, alter folate and B12 levels, and perhaps influence hypothalamic releasing hormone levels. The level of serotonin is influenced in the following manner. The estrogens in oral contraceptives increase tryptophan available for the brain to convert to serotonin and tryptamine. Depression is associated with lower levels of serotonin, tryptamine, and perhaps tryptophan in the brain. Estrogens in oral contraceptives may also alter pryridoxal phosphate which in turn affects the production of serotonin. Oral contraceptives possibly lower norepinephrine levels by 1) decreasing tyrosine; 2) influencing coenzymes necessary to norepinephrine production; and 3) increasing monoamine oxidase levels. Oral contraceptives apparently inhibit the metabolism of folate and B12, and lower levels of these substances are associated with depressive symptoms. Decreased norepinephrine and serotonin levels may inhibit the release of gonadotrophin-releasing hormones, and these hormones may in turn influence behavior. Recommendations to clinicians were: 1) patients should be screened for a history of depression prior to prescribing oral contraceptives; 2) pill users should be monitored for depression; and 3) 25 mg daily of pyxidoxine should be administered if a patient taking oral contraceptives is deficient in B6.
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PMID:Oral contraceptives and depressive symptomatology: biologic mechanisms. 3 42

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

An experimental model resembling so-called tropical sprue has been produced in young, growing rhesus monkeys kept on a protein-deficient diet. At a 2% level of protein intake, the animals became frankly diseased after two months, but at a 5% protein intake the symptoms appeared after five months. The animals lost weight, their skin became brittle, the fur lost luster, and facial edema appeared. The hematocrit, and serum folate, protein and albumin were significantly decreased, and intestinal absorption of fat, D-xylose, radioactive vitamin B12 and folic acid showed marked depression. The jejunal mucosa showed moderate villous atrophy. Histochemical and electron microscopy changes were consistent with those seen in the human tropical sprue syndrome. It appears, therefore, that protein malnutrition plays an important role in the experimental tropical-sprue-like syndrome in monkeys.
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PMID:Primate model of sprue-like syndrome. 10 18

The uptake of vitamin B12 was measured in cells of Escherichia coli whose growth had been inhibited by any of a variety of treatments. In all cases, the secondary, energy-dependent phase of B12 uptake was depressed in proportion to the decrease in growth rate, but uptake was constant in cells growing logarithmically at different rates. The depression of B12 uptake activity was independent of the site of cell metabolism affected by the inhibitor or by its effect on cell viability, and was both more rapid and of greater degree than the effects on the uptake of any of the six amino acids tested. The decline was not affected by inhibitors of either cell division or proteolysis and was manifested without any apparent decrease in the surface B12 binding activity. Transport activity was rapidly regained upon reversal of the inhibition of protein synthesis. Prompted by this response, the uptake of B12 was contrasted to the apparent uptake of the E colicins, which share the same outer membrane receptor. Sensitivity to colicin E1, measured by its inhibition of proline uptake, was not affected by growth inhibition by antibiotic treatment. Finally, there was no specific depression of B12 uptake in cells rendered colicin tolerant either by mutation or as a consequence of phage f1 infection.
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PMID:Relation of cell growth and colicin tolerance to vitamin B12 uptake in Escherichia coli. 31 41

Recent reports demonstrated that the energy-dependent step of vitamin B12 uptake into cells of Escherichia coli rapidly declines after cessation either of the expression of the tonB gene or of general protein synthesis. It is shown here that inhibition of protein synthesis results in the decline, with similar kinetics, of all tonB-dependent processes, including sensitivity to colicins B and Ia, irreversible adsorption of phage phi80, and siderophore-mediated iron uptake. The role of ongoing TonB-dependent reactions on this lability of TonB function was investigated. Ferrichrome and the enterochelin precursor, 2,3-dihydroxybenzoate, caused both a moderate depression of B12 uptake activity in growing cells (reversed upon removal of the siderophore) and an acceleration of the loss of activity following inhibition of protein synthesis by addition of spectinomycin. Strains lacking the tonB-dependent siderophore uptake systems did not show these responses. The results suggest the consumption of tonB product during its action.
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PMID:Outer membrane-dependent transport systems in Escherichia coli: turnover of TonB function. 35 Aug 36

Growth of Escherichia coli K-12 strains in the presence of the vitamin cyanocobalamin (B12) resulted in an 80 to 90% reduction in B12 uptake activity of washed cells. Coincident with the decline in uptake activity was the depression of B12-binding activity in energy-poisoned cells, suggesting that growth in B12 resulted in the repression of synthesis of the B12 receptor protein in the outer membrane. Growth in the presence of B12 led to marked reduction in sensitivity to the E colicins, whose adsorption to cells requires the B12 receptor, and to a decrease in the amount of a band on electropherograms of outer membrane proteins. That polypeptide was also missing from mutants altered at btuB, the locus encoding the B12 receptor. Addition of B12 to growing cultures resulted in the exponential decline in specific activity of B12 uptake, as expected for dilution of functional receptors by further growth. Repression of receptor synthesis appears to be regulated by the level of intracellular, rather than extracellular, B12 and is separate from the regulation of the methionine biosynthetic pathway. Mutants altered in btuC, which are defective in accumulation and retention of B12, exhibit a much lower degree of repressibility.
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PMID:Repression of synthesis of the vitamin B12 receptor in Escherichia coli. 36 85

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

Two experiments examined whether vitamin B12 status of liver affects milk fat percentage or yield. In Experiment 1 B12 concentration in liver, measured at approximately 8 and 15 wk postpartum in 35 cows, was not correlated significantly with milk fat percentage or yield. In Experiment 2 twenty-two cows were fed a ratio similar to one used to depress milk fat percentage. The B12 status of 12 of these cows was enhanced by intramuscular injection of vitamin B12 while the other 10 served as controls. During wk 2 to 8 of lactation, milk fat percentages were almost identical for the two groups. A difference in milk fat yield in favor of the B12-treated group resulted from a difference in milk yield. The data do not support a recent hypothesis of the metabolic cause of milk fat depression.
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PMID:Milk fat as related to vitamin B12 status. 45 90

Oral contraceptive (OC) use has been associated with 50 different metabolic changes but few women require increased amounts of nutrients to prevent deficiencies. Plasma triglyceride levels are markedly increased by OCs, but no consistent changes have been found in plasma cholesterol, fatty acids, or phospholipids. Small elevations in blood glucose and plasma insulin levels result from OC use, and plasma albumin is decreased and the alpha and beta globulins and fibrinogen are increased. Women on the pill show slight increases in the urinary excretion of some of the amino acids and decreases in some of the blood amino acids. Tryptophan metabolism is altered by OC use; changes in parameters of Vitamin-B6 metabolism are seen and Vitamin-B6 is used as a cofactor for several enzymes in the tryptophan pathway. At the beginning of OC use the retention of dietary nitrogen increases, and weight gain may result. The estrogens in OCs reduce plasma calcium, phosphorus, and magnesium. Most studies demonstrate an increase in serum iron and copper and a decrease in plasma zinc. Studies have also found an increase in plasma levels of Vitamin-A and a decrease of carotene, Vitamin-E, ascorbic acid, folacin, Vitamin-B12, and Vitamin-B6. 20% of OC users have enlarged cervical and vaginal cells as a result of abnormal folacin metabolism. The abnormality is corrected by oral folacin supplementation. Some women respond to OC treatment with biochemical signs of Vitamin-B6 deficiency and depression. These women should receive 20-40 mg Vitamin-B6 as a supplement.
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PMID:Nutrition during oral contraceptive treatment. 58 16

Serum folate and B12 estimations were carried out on 272 admissions to a psychiatric unit during 1972 and 1973. 21.3% had serum folate below 2 ng/ml and 26.1% serum B12 below 150 pg/ml. The organic psychosis patients had a significantly lower mean B12 than the others, and were over-represented among the low B12 group. Low B12 status was also associated with low RBC and WBC. Low folate status was linked with depression, malnutrition, physical illness and low Hb, RBC and WBC. There were more chronic alcoholics than others with serum folate greater than 4-9 ng/ml, low RBC and macrocytosis. The presence of one or more haematological abnormalities (macrocytosis, low Hb, low RBC or low WBC) predicted low folate in 76%, and low B12 in 79%, but these were also found in 40% of the normal folate and 41% of the normal B12 patients. Macrocytosis may prove to be a reliable sign of alcoholic abuse.
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PMID:Serum folic acid and B12 in 272 psychiatric in-patients. 63 65


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