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)

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

1. For methods of vitamin E and selenium supplementation were evaluated using thirty-nine pregnant ewe-lambs fed on a ration containing 0.043 mg Se/kg and 25 mg vitamin E/kg. Treatments were control, fortified mineral mix (ESe salt) (300 mg vitamin E, 3 mg Se), ruminal Se pellets (505 mg Se), drench (300 mg vitamin E, 3 mg Se) and intramuscular injection (600 mg vitamin E, 3 mg Se). Only ewes supplemented, commencing approximately 50 d before parturition. 2. Birth weights were similar for all treatments and live-weight gains of lambs to 56 d of age were improved in all supplemented groups (P less than 0.05). There were no clinical cases of nutritional muscular dystrophy. 3. Se concentrations in whole blood were more than doubled in both lambs and ewes drenched or injected; responses to ESe salt and pellets were much smaller. 4. Plasma tocopherol levels were increased in injected dams and their lambs (P less than 0.001). 5. Haemoglobin concentration and erythrocyte counts were significantly higher (P less than 0.01) in control ewes and lambs than in treated lambs. 6. Lactate dehydrogenase (EC 1.1.1.27), creatine kinase (EC 2.7.3.2) and aspartate aminotransferase (EC 2.6.1.1) activities were increased in lambs from control, ESe salt and pellet groups (P less than 0.001). Glutathione peroxidase (EC 1.11.1.9) activity responded to Se supplementation in both ewes and their lambs (P less than 0.001) and the response was highest in the injected group, followed in order, by the drench, pellet, Ese salt and control groups. 7. These studies indicated that in terms of the haematological and blood chemistry changes investigated, the intramuscular injection was most effective, followed by the oral drench. Ruminal pellets and fortified salt were less satisfactory.
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PMID:Haematological and blood chemistry changes in ewes and lambs following supplementation with vitamin E and selenium. 69 59

Pigs which were deficient in vitamin E and/or selenium had the following parameters weekly determined from six to 13 weeks of age: Packed cell volume, hemoglobin concentration, red cell and white cell counts, red cell indices, reticulocyte count, serum iron, serum total iron binding capacity, myeloid: erythroid ratio, serum glutamic-oxaloacetic transaminase and creatine phosphokinase activities and body weight. Except for the myeloid:erythroid ratio and serum creatine phosphokinase activity, these parameters were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency of both. The myeloid:erythroid ratio was increased (p less than 0.01) in association with selenium deficiency, which tends to indicate decreased erythropoiesis but was not reflected in the peripheral red cell picture. Evidence of dyserythropoiesis was not found to be a significant feature in serial bone marrow aspiration biopsies of vitamin E and/or selenium deficient pigs. Even if the serum glutamic-oxaloacetic transaminase activities were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency in both as compared to replete animals, a few animals, especially in the group deficient in both vitamin E and selenium, presented quite marked transient increases of serum glutamic-oxaloacetic transaminase activity which was interpreted to reflect the occurrence of acute episodes of hepatosis dietetica. Serum creatine phosphokinase activities were found to be increased in association with vitamin E deficiency (p less than 0.01), selenium deficiency (less than 0.05) and the interaction was also significant (p less than 0.01). It was concluded that the serum creatine phosphokinase activity increases reflect the occurrence of subclinical muscular dystrophy and that vitamin E and selenium deficiencies have marked additive effects in the induction of skeletal muscular dystrophy.
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PMID:Studies on vitamin E and selenium deficiency in young pigs. I. Hematological and biochemical changes. 83 88

Rabbits were fed a vitamin E-deficient diet for 7 weeks. Control rabbits, paired for weight, were pair-fed an identical diet supplemented with vitamin E. After 3 weeks the expermental animals showed a rise in serum creatin kinase activity which was attributable to the muscle isoenzyme (MM). No rise in creatine kinase activity or appearance of MM was noted in the serum of the control rabbits. Total creatine kinase activity and MM activity were reduced in the gastrocnemii of the experimental animals while the activities of the brain (BB) and hybird (MB) isoenzymes were increased. The specific activity of BB based on immunochemically determined BB protein was not different from normal in either the experimental or control group. Activation of pre-existing inactive BB is probably not the explanation for increased BB activity in the gastroncnemii of the experimental group.
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PMID:Brain isoenzyme of creatine kinase. III. Active and inactive forms in dystrophic muscle of vitamin E-dificient rabbit. 86 75

Three 2 X 2 factorial experiments were conducted with sheep fed purified diets to determine the effects of selenium and vitamin E on the incidence of white muscle disease (WMD) and blood components. All lambs reaching 6 weeks of age in the group receiving no vitamin E or selenium developed WMD lesions, whereas only a few lambs in either the +E - Se or -E + Se treatment groups developed these lesions. Plasma activities of creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase were significantly elevated in lambs receiving no vitamin E or selenium, whereas these enzyme activities in those receiving only selenium were non-significantly elevated. The enzyme activities in plasma of those on the +E - Se or +E + Se treatments were maintained at low levels, suggesting vitamin E alone is more effective in preventing WMD than selenium alone. The metabolic interactions of these essentials are discussed.
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PMID:Effects of selenium and vitamin E deficiencies on reproduction, growth, blood components, and tissue lesions in sheep fed purified diets. 87 72

One of group of pregnant Holstein-Friesian heifers became recumbent the day after it was transported approximately 100 km. The heifer died after 10 days of recumbency, in spite of symptomatic treatment, which included an injection of a selenium-vitamin E (Se-E) preparation on day 5. Serum creatine phosphokinase activity was 21,000 IU/L on day 3 and 6,290 IU/L on day 9. Gross and histopathologic findins were characteristic of Se-E deficiency. Hepatic selenium content on day 10 was low (0.13 ppm) in spite of the Se-E injection given earlier.
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PMID:Myodegeneration associated with selenium-vitamin E deficiency in a pregnant heifer. 90 89

Two experiments to study nutritional muscular dystrophy (N.M.D.) in calves were conducted in northern Ontario, where the disease is prevalent. In the first experiment, ninety Shorthorn cows were used. They were divided into three groups and fed the following forages during the winter of 1972-1973. Group I - Silage. Group II. - Heated-air-dried hay. Group III. - Field-dried hay. Chemical analysis of the forage during storage showed that the silage had a higher tocopherol content than the other two forages. This higher content had a direct effect on plasma tocopherol concentrations in the cows, since tocopherol levels were found to be higher in the group fed silage than in the other two groups. The highest mortality rate-eight dead calves-was in the group fed heated-air-dried hay; one calf died in each of the other two groups. Hence, it is evident that the severity of N.M.D. symptoms in calves is directly linked with the quantity of selenium or vitamin E ingested. The substances act synergistically to protect against the disease. In a second experiment, a herd of forty-seven Shorthorn cows, some of which had calves with N.N.D. and some of which had healthy offspring, were studied to measure the activity of serum creatine phosphokinase. The dams were found to have the same C.P.K., whether or not their calves suffered from N.M.D.
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PMID:[Vitamin E activity of stored forages and incidence of myopathy in calves]. 103 40

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

Seventy-eight newborn pigs were allotted to 4 treatment groups: 22 pigs in group A were given no selenium-vitamin E (Se-E), 22 pigs in group B were given small doses of Se-E, 22 pigs in group C were given medium doses of Se-E, and 12 pigs in group D were given large doses of Se-E. Pigs were intramuscularly injected before 7 days of age and at weaning (40 days of age), respectively, as follows: group A--1 ml of physiologic saline solution/pig each time, group B--0.25 mg of Se/pig and later 0.06 mg of Se/kg of body weight, group C--1.0 mg of Se/pig and later 0.24 mg of Se/kg, and group D--1.5 mg of Se/pig and later 0.72 mg of Se/kg. Selenium was supplied as sodium selenite in commercially available Se-E injectable compounds. From 2 weeks of age to weaning, the pigs were fed a corn-torula yeast creep feed containing Se at the concentration of 0.03 ppm, and from weaning to slaughter, a corn-soybean meal ration was fed containing Se at the concentration of 0.07 ppm and alpha-tocopherol at the concentration of 15.7 mg/kg. Subclinical Se-E deficiency developed in control pigs of group A and was characterized by subtle muscular stiffness, significant increases in plasma activities of glutamic oxalacetic transaminase (GOT) and creatine phosphokinase (CPK), and typical residual lesions in heart and skeletal muscle, but not in liver, at slaughter at 165 days of age. Pigs injected with Se-E did not develop these evidences of subclinical deficiency. Pigs in group D were stunted for several weeks after the 2nd Se-E injection, and plasma GOT and CPK activities were significantly increased at 3 weeks after injection. Growth rates were otherwise similar between groups. Significant difference in Se content of liver, muscle, serum, and hair was not seen between pigs in the 4 groups at 120 and 165 days of age. A test period of physical exertion and heat stress resulted in significant increase of plasma GOT and CPK activities in 4 of 8 pigs at 110 days of age.
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PMID:Efficacy and safety of selenium-vitamin E injections in newborn pigs to prevent subclinical deficiency in growing swine. 112 75

Young male rats were fed diets containing 20 per cent fat in the form of soybean oil, corn oil, safflower oil, or hydrogenated shortening, and their vitamin E status was assessed for twenty-seven weeks. On the basis of growth rate, in vitro red cell hemolysis, plasma creatine phosphokinase activity, and testicular development, soybean oil, corn oil, and shortening provided adequate vitamin E. Rats fed safflower oil had slight red cell hemolysis but were normal in other respects. When the tocopherols in corn oil were reduced by half, vitamin E status still appeared normal. Tissue levels of alpha- and gamma-tocopherols were determined in all groups, and the limitations of the dietary E:PUFA ratio are discussed.
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PMID:Vitamin E adequacy of vegetable oils. 116 55


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