Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liposomes were prepared from phospholipids extracted from biological membranes. A comparison was made between the peroxidation rate in handshake liposomes and in sonicated liposomes. The smaller sonicated liposomes were more vulnerable to peroxidation, probably because of the smaller radius of curvature, which results in a less dense packing of lipid molecules in the bilayer and a facilitated action of water radicals produced by the X-irradiation. High oxygen enhancement ratios were obtained, especially at low dose rates, suggesting the operation of slowly progressing chain reactions initiated by ionizing radiation. Three compounds were tested for their ability to protect the liposomal membranes against lipid peroxidation. The naturally occurring compounds reduced glutathione (GSH) and vitamin E(alpha-T) and the powerful radiation protector cysteamine (MEA). All three molecules could protect the liposomes against peroxidation. The membrane-soluble compound vitamin E was by far the most powerful. About 50 per cent protection was achieved by using 5 X 10(-6) M alpha-T, 10(-4) M GSH and 5 X 10(-4) M MEA. The fatty acid composition of the lipids altered drastically as a result of the irradiation. Arachidonic acid and docosahexanoic acid were the most vulnerable of the fatty acids. Very efficient protection of these polyunsaturated fatty acids could be obtained with relatively low concentrations of vitamin E built into the membranes.
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PMID:Protection of liposomal lipids against radiation induced oxidative damage. 31 91

We observed the levels of vitamin E in the blood serum of calves after peroral application of Combinal E (1 ml contains 20 mg of tocopherol acetate in water solution), after application through a fistula into the rennet stomach and after an intramuscular injection of Erevit (1 ml contains 300 mg of tocopherol acetate in vegetable oil). The fastest increase in the vitamin E level was recorded after the application of Combinal E directly into the rennet stomach. The application of Combinal E per os resulted in the same level of vitamin E in the ninth hour after application as in the third hour after application into the rennet stomach, the intramuscular injection of Erevit had a much lower effect on raising the vitamin E level in the blood serum of calves. It was confirmed that for a faster supplementing of vitamin E to the organism it is more suitable to give Combinal E perorally.
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PMID:[Vitamin E serum levels in calves after various methods of administration]. 41 Dec 12

This paper describes a rapid, microprocedure for the simultaneous determination of alpha-tocopherol (vitamin E) and retinol (vitamin A) in plasma, and of alpha-tocopherol alone in red cells since cells do not contain retinol. A total lipid extract from 0.1 ml plasma or 0.125 ml red cells and containing internal standards of alpha-tocopheryl acetate and retinyl acetates is injected onto a high pressure liquid chromatography with a reverse phase column developed with methanol-water. An ultraviolet detector with 280-nm filter is used. The chromatogram is complete in 8 min and the alpha-tocopherol and retinol are quantitated by the peak height ratio method. Comparison of results with both plasma and red cells gave excellent agreement with conventional methods for these vitamins. The procedure should be particularly useful for clinical studies and nutrition surveys.
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PMID:Simultaneous determination of alpha-tocopherol and retinol in plasma or red cells by high pressure liquid chromatography. 48 33

Although a neuromuscular syndrome has been induced experimentally by vitamin E deficiency, a human syndrome has not yet been documented. This report describes a 7-year-old boy with severe malabsorption since birth who presented with progressive external ophthalmoplegia, proximal muscle weakness, peripheral neuropathy, hyporeflexia, and bilateral Babinski signs. Abnormalities on neurologic examination included elevated creatine phosphokinase and aldolase, slowed distal sensory latencies, type II muscle fiber atrophy, and a plasma vitamin E level of 8 microgram per deciliter (normal, 550-1500 microgram per deciliter). Treatment with oral water-solubilized vitamin E (400 IU daily; greater than 50 times the normal daily intake) was begun, with repeat laboratory studies at 3-month intervals. Over a 16-month period, plasma vitamin E content gradually increased to 350 microgram per deciliter, associated with declining sarcoplasmic enzyme activities and clinical improvement.
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PMID:Reversibility of human myopathy caused by vitamin E deficiency. 57 10

Experiments were conducted to evaluate the utilization of d1-alpha-tocopherol, d1-alpha-tocopheryl acetate and a water-soluble ester, d-alpha-tocopheryl polyethylene glycol 1000 (TPGS), as dietary sources of vitamin E for the chick. Results showed that tocopheryl acetate is utilized with efficiency equal to that of vitamin E alcohol at dietary concentrations less than or equal to approximately 40 ml d1-alpha-tocopherol equivalents per kg. At greater dietary concentrations of the vitamin, the alcohol form appeared to be better utilized than the acetate when it was adequately stabilized in the diet. However, TPGS was poorly utilized at all dietary levels examined. Saponification of both esters improved the utilization of vitamin E from these sources. The utilization of all forms of vitamin E was depressed in hypervitaminotic A chicks and, to a lesser extent, in chicks fed ethoxyquin.
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PMID:Studies on the utilization of vitamin E alcohol and esters by the chick. 67 9

Supplemental vitamin E is extracted from feed in one step with methanol and analyzed by reverse phase partition chromatography in less than 10 min, using isocratic elution with either methanol or water-methanol as the mobile phase. Detection response (as measured by peak area) was linear between 0.5 and 3.0 mug, and the coefficients of variation for retention time and peak height on replicate analyses of the standard sample were 0.8 and 2.3%, respectively.
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PMID:High performance liquid chromatographic analysis of supplemental vitamin E in feed. 83 88

Weanling male rats were fed either a vitamin E-deficient Torula yeast diet fortified with selenium or the same diet supplemented with 100 ppm vitamin E. One group of rats fed each diet received plain distilled water, whereas another group received 250 ppm lead as lead acetate in the drinking water. After a 3 month feeding period, erythrocyte osmotic and peroxidative fragilities were determined in an osmotic test recorder. Dietary vitamin E had little or no effect on the osmotic fragility of red cells. Lead in the drinking water, however, decreased the osmotic fragility of red cells from deficient rats. Lead poisoning also markedly decreased the elevated peroxidative fragility characteristic of erythrocytes from vitamin E-deficient rats. This effect of lead in reducing the peroxidative fragility of red cells from deficient rats could be seen at levels as low as 25 ppm lead in the drinking water. Lead added in vitro decreased the peroxidative fragility of red cells from vitamin E-deficient non-poisoned rats, whereas neither mercury nor cadmium had such an effect. Lead may decrease the osmotic and peroxidative fragility of erythrocytes from vitamin E-deficient rats by "tanning" the red cell membrane. These results suggest that the peroxidative fagility test as carried out with an osmotic test recorder may not be a valid indicator of the vitamin E status of animals exposed to lead.
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PMID:Osmotic and peroxidative fragilities of erythrocytes from vitamin E-deficient lead-poisoned rats. 84 74

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.
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PMID:Comparative effects of selenium and vitamin E in lead-poisoned rats. 84 75

The role of vitamin E in human nutrition was studied by investigation of patients with cystic fibrosis (CF) and associated pancreatic insufficiency. Vitamin E status was assessed by measurement of the plasma concentration of the principal circulating isomer, alpha-tocopherol. Results of such determinations in 52 CF patients with pancreatogenic steatorrhea revealed that all were deficient in the vitamin. The extent of decreased plasma tocopherol varied markedly but correlated with indices of intestinal malabsorption, such as the serum carotene concentration and percentage of dietary fat absorbed. Supplementation with 5-10 times the recommended daily allowance of vitamin E in a water-miscible form increased the plasma alpha-tocopherol concentrations to normal in all 19 CF patients so evaluated. Studies on the effects of vitamin E deficiency focused on possible hematologic alterations. An improved technique was developed to measure erythrocyte hemolysis in vitro in the presence of hydrogen peroxide. While erythrocyte suspensions from control subjects demonstrated resistance to hemolysis during a 3-h incubation, all samples from tocopherol-deficient CF patients showed abnormal oxidant susceptibility, evidenced by greater than 5% hemoglobin release. The degree of peroxide-induced hemolysis was related to the plasma alpha-tocopherol concentration in an inverse, sigmoidal manner. The possibility of in vivo hemolysis was assessed by measuring the survival of (51)Cr-labeled erythrocytes in 19 vitamin-E deficient patients. A moderate but statistically significant decrease in the mean (51)Cr erythrocyte half-life value was found in this group. Measurement of erythrocyte survival before and after supplementation of 6 patients with vitamin E demonstrated that the shortened erythrocyte lifespan could be corrected to normal with this treatment. Other hematologic indices in deficient subjects, however, were normal and did not change upon supplementation with vitamin E. It is concluded that CF is invariably associated with vitamin E deficiency, provided that the patient in question has pancreatic achylia and is not taking supplementary doses of tocopherol. Concomitant hematologic effects consistent with mild hemolysis, but not anemia, occur and may be reversed with vitamin E therapy. Patients with CF should be given daily doses of a water-miscible form of vitamin E to correct the deficiency.
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PMID:The occurrence and effects of human vitamin E deficiency. A study in patients with cystic fibrosis. 87 86

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.
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PMID:Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs. 93 27


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