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)

Because of previous reports of the beneficial effect of vitamin E in angina pectoris patients, 48 patients, with both stable angina and positive (chest pain plus ishemic ST depression) maximal exercise treadmill tests, participated in a double-blind cross-over study of 6 months of vitamin E and 6 months of placebo therapy, separated by a 2 month no treatment period. All 48 patients had positive selective coronary arteriograms (75 per cent obstruction of at least a major coronary artery) and/or Q wave ECG evidence of previous myocardial infarction (Minnesota criteria). Evaluation of drug effectiveness was based on performance of serial maximal exercise treadmill tests, serial systolic time interval measurements, and daily angina diaries. No statistically significant differences between the two treatment studied. It is concluded that a large dose of vitamin E (1,600 I.U. of d-alpha-tocopherol succinate daily) for 6 months in patients with stable angina pectoris fails to increase the exercise capacity, improve left ventricular function, or reduce the frequency of chest pain.
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PMID:Quantitative evaluation of vitamin E in the treatment of angina pectoris. 32 Aug 56

The effect of oxygen (O2) exposure on the ability of the isolated, perfused rat lung to clear serotonin (5-hydroxytryptamine, 5-HT) from the perfusate was evaluated in normal or vitamin E-deficient Sprague-Dawley rats. Rats were exposed to 100% O2 at 1 ATA for 4-48 h. Lungs were subsequently isolated, artificially ventilated, and perfused in a recirculating system with Krebs-Ringer bicarbonate solution, pH 7.4 containing 3% bovine serum albumin and 0.25 muM [14C] 5-HT. 5HT clearance was calculated from the disappearance rate of [ 14C] 5-HT from the perfusate. In normal rats exposed to 100% O2, there was a progressive reduction in the clearance of 5-HT with increasing duration of O2 exposure. Compared to lungs from air-exposed controls, clearance was depressed 20% (P less than 0.01) after 18 h, 22% (P less than 0.01) after 24 h, and 35% (P less than 0.001) after 48 h. With vitamin E-deficient rats, the reduction in 5-HT clearance occurred after a shorter exposure time and was of greater magnitude than in rats on a normal diet. Depression of 5HT clearance by the lungs is an early alteration of lung function fue to hyperoxia and is potentiated by vitamin E deficiency. The most likely mechanism for the depression of 5-HT clearance is interference with the transport properties of lung endothelium.
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PMID:Depression of serotonin clearance by rat lungs during oxygen exposure. 83 74

The effect of dietary vitamin E on lipid synthesis from U-14 C-D-glucose and 1-14C-acetate was studied in rat lungs in vitro. One-month-old Sprague-Dawley male rats were fed either a basal vitamin E-deficient diet or one supplemented with 45 ppm vitamin E ad libitum for two months. Glucose oxidation to CO2 by lungs was significantly (p less than 0.05) decreased by the exclusion of vitamin E from the diet. Oxidation of acetate to CO2 was not affected by the presence of vitamin E in the diet. The extent of labeled carbons from both glucose and acetate incorporated into total lipids was significantly lower in the lungs of vitamin E-deficient animals than in those of the supplemented group. However, the relative amounts of phospholipids, neutral lipids are free fatty acids in total lipids, and of glyceryl moiety and fatty acids in total lipids and in phospholipid fraction were not significantly altered by the status of dietary vitamin E. The results suggest a general depression of lipid synthesis in the lungs of vitamin E-deficient rats.
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PMID:Effect of dietary vitamin E on lipid synthesis by rat lung in vitro. 84 45

Clearance of 5-hydroxytryptamine (5-HT) by the lungs of normal and vitamin E-deficient rats was evaluated following a 60-min exposure to 100% oxygen (O2) at 4 ATA (HBO). After exposure, lungs were isolated, ventilated, and perfused, with a recirculating system used for measurement of 5-HT clearance. Control lungs were obtained from rats exposed to air at 1 ATA. In control normal rats, fractional clearance of 5-HT was 0.78+/-0.03 (mean+/-SE). Following HBO 5-HT clearance was 0.55+/-0.04 (P less than 0.01). In control vitamin E-deficient rats. 5-HT clearance was 0.85+/-0.05 and was decreased to 0.46+/-0.03 (P less than 0.001) following HBO. To evaluate the effect of recovery time after HBO on 5-HT clearance, separate groups of rats were killed at varying intervals post-HBO. In normal rats, 5-HT clearance had returned to control levels by 3-4 after HBO; in vitamin E-deficient rats, clearance remained unchanged 4 h after HBO and was only 74% (P less than 0.001) of control values 24 h post-HBO. These results indicate that depression of pulmonary 5-HT clearance occurs in rats due to hyperoxia and is potentiated by vitamin E deficiency. This represents a reversible alteration of lung function which requires vitamin E for complete recovery.
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PMID:Effect of hyperbaric oxygen exposure on pulmonary clearance of 5-hydroxytryptamine. 89 79

Four weanling swine fed for 4 weeks a commercial ration adequate in selenium and vitamin E, but supplemented with 0.5% silver acetate, developed lesions typical of selenium-vitamin E deficiency. Clinically, the pigs fed this high level of silver had anorexia, diarrhea, and growth depression; 3 of 4 pigs died. At necropsy, hepatic lesions of hepatosis dietetica were present in 4 of 4 silver-fed pigs, and 1 of 4 pigs had cardiac and skeletal muscle lesions characteristic of selenium-vitamin E deficiency. Development of lesions and mortality was prevented in 2 pigs fed the silver diet supplemented with alpha-tocopherol (100 IU/kg of diet), but not in 2 pigs fed the ration supplemented with selenium as selenite (1 ppm). Four pigs fed a lower dose level of silver (0.2% silver acetate) for 6 weeks failed to develop clinical or pathologic features of selenium-vitamin E deficiency. However, hepatic selenium content was significantly increased in pigs fed the silver-supplemented ration.
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PMID:Induction of lesions of selenium-vitamin E deficiency in pigs fed silver. 99 68

Eight 5-to 8-week-old Beagle pups were allotted to 4 groups of 2 dogs each. For 55 to 70 days, they were fed either a semisynthetic basal diet (BD) deficient in vitamin E and selenium (Se) (group 1) or the BD supplemented with either 30 IU alpha-tocopherol/kg (group 2), 0.5 ppm Se as selenite (group 3), or 1.0 ppm Se as selenite (group 4). In the dogs fed the BD, clinical signs of vitamin E-Se deficiency developed after 40 to 60 days. These signs were accompanied by increased plasma activity of creatine phosphokinase (CPK) and glutamic oxalacetic transaminase (GOT). The dogs were euthanatized after 10 to 15 days of progressive clinical signs, including muscular weakness, subcutaneous edema, anorexia, depression, dyspnea, and eventual coma. Gross lesions seen at necropsy included ventral subcutaneous edema, generalized skeletal muscular pallor and edema with scattered white longitudinal streaking, prominent brownish yellow discoloration of the intestinal musculature, and a layer of white chalky material at the renal corticomedullary junction. Microscopically, there was evidence of extensive skeletal muscular degeneration and regeneration, focal subendocardial necrosis in the ventricular myocardium, intestinal lipofuscinosis, and renal mineralization. Mean hepatic Se content in the dogs fed the BD was 0.10 ppm (wet weight basis) at necropsy. In the dogs fed the 3 supplemented diets, clinical signs of deficiency did not develop. At necropsy, mild skeletal myopathy was evident histologically in the dogs fed BD and 0.5 ppm Se (group 3) but not in the dogs fed the other supplemented diets. Intestinal lipofuscinosis was found in the dogs fed the 3 supplemented diets but was less severe in the dogs fed the diet supplemented with vitamin E than in those fed diets supplemented with Se.
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PMID:Experimentally induced vitamin E-selenium deficiency in the growing dog. 112 Jul 35

Dietary Se (0.5 ppm Se supplied as sodium selenite to a casein-based diet containing 0.02 ppm Se and lacking in vitamin E) prevented the growth depression observed in rats receiving 76 ppm Ag in the water supply and markedly improved growth and survival of those given 751 ppm Ag. The Ag concentration of liver and possibly of kidney was increased by Se. Liver glutathione peroxidase activities from rats fed 0.5 ppm Se and given 76 and 751 ppm Ag for 52 days in their water were, respectively, 30% and 4% of those from control rats fed 0.5 ppmSe without Ag. In rats fed a diet, adequate in vitamin E (100 IU/kg) and Se (0.5 ppm as sodium selenite), administration of 751 ppm Ag in the water for 15 wk reduced liver GSH-Px activity to 5% of that from control rats receiving no Ag. GSH-Px activity of erythrocytes and kidney was decreased by Ag to 37% and 38%, respectively, of control values. It is concluded that in vivo administration of Ag dramatically decreased liver GSH-Px in rats fed Se-supplemented diets with or without vitamin E. Furthermore, supplemental Se (0.5 ppm) prevented the growth depression and mortality caused by Ag in rats fed a diet lacking vitamin E, while increasing the Ag concentration of liver and kidney.
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PMID:Alleviation of silver toxicity by selenite in the rat in relation to tissue glutathione peroxidase. 112 24

Two experiments were conducted with chicks to compare the effectiveness of vitamin E,selenium and cystine in preventing the deleterious effects of dietary silver. Adding 900 p.p.m. silver to a diet marginal in vitamin E and selenium significantly depressed growth and caused a high mortality during the four-week experiment. Most of the mortality was due to exduative diathesis. Including either 1 p.p.m. selenium or 100 I.U. vitamin E per kg. in the diets with silver prevented the growth depression and mortality. Adding 0.15% cystine stimulated growth, but failed to rpevent mortality. In a second experiment, chicks were grown on the diet containing silver with and without cystine to 15 days of age, at which time approximately 50% of the chicks exhibited signs of exudative diathesis. At that time they were either continued on the same diet of fed diets supplemented with selenium or vitamin E. Both vitamin E and selenium reduced mortality during the following two-week period, but vitamin E. was more effective than selenium.
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PMID:Induced exudative diathesis in chicks by dietary silver. 115 78

Male Sprague-Dawley rats maintained for a period of 6 or 12 weeks on a basal vitamin E-dificient diet consisting of 70% sucrose, 20% vitamin-free casein, 4% tocopherol stripped lard, 4% salt mixture, and 2% tocopherol-free vitamin fortification mixture were used to compare two sets of commonly used salt mixtures (salt mixtures USP XIV versus Briggs' salt mixture) and two sets of vitamin fortification mixtures (NBC vitamin fortification mixture versus that of Weglicki). Among the rats maintained on the deficient diets for 6 weeks, only those that received the combination of salt mixture USP XIV and vitamin fortification mixture of Weglicki showed a significantly lower level of hepatic catalase activity compared to the corresponding control animals. While there were no significant changes in microsomal cytochromes at this time period, after 12 weeks on the deficient diet, a significant depression in these cytochromes was noted in all experimental groups except the one on salt mixture USP XIV and NBC vitamin fortification mixture. A similar decrease in hepatic catalase was observed in deficient animals at 12 weeks. Since the most striking differences in these diets are in their content of iron and menaquinone, it appears that these two dietary constituents may interact in modulating the effect of vitamin E on hepatic hemeproteins.
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PMID:Effects of different vitamin E-deficient basal diets on hepatic catalase and microsomal cytochromes P-450 and b5 in rats. 118 Feb 43

Red deer calves dying at 24 to 72 hours old were infected with cryptosporidia. The clinical signs were extreme depression and weakness, but they did not consistently have diarrhoea. One calf was severely uraemic, and evidence from subsequent cases suggested that cryptosporidium infection in very young red deer calves may result in terminal uraemia. The possibility of intrauterine infection is considered. The factors which could have predisposed to the outbreak of infection were investigated; the calves were deficient in vitamin E despite having received adequate colostrum.
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PMID:Cryptosporidiosis in newborn red deer (Cervus elaphus). 156 43


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