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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a newly developed lipid peroxidation-inducing system composed of DOPA and iron, we examined the vulnerability of substantia nigra to peroxidation in comparison with that of caudate-putamen obtained from normal or vitamin E-deficient animals. Histochemical detection of lipid peroxidation revealed that substantia nigra was far more susceptible than caudate putamen to DOPA and iron treatment, which was biochemically supported by measurements of thiobarbituric acid-reactive substances. Vitamin E deficiency accelerated such susceptibility of substantia nigra but had no influence on the histochemical findings observed in caudate-putamen.
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PMID:Combined histochemical and biochemical demonstration of nigral vulnerability to lipid peroxidation induced by dopa and iron. 140 98

A 33-day feeding experiment was conducted with 3-day-old broiler chicks to assess the efficacy of various flavonoid and simple phenolic antioxidants in preventing nutritional muscular dystrophy (NMD) resulting from vitamin E deficiency. None of the flavonoids or simple phenolics at a dietary concentration of 1,000 ppm completely prevented NMD but quercetin reduced (P less than .05) its incidence and quercetin, morin, and ferulic acid reduced (P less than .05) the severity of the disorder. The low-selenium, low-vitamin E diet also promoted the development of a mild exudative diathesis (ED) in many of the birds, which was inhibited (P less than .05) by the rutin and silymarin treatments, but exacerbated (P less than .05) by quercetin, morin, and ferulic acid. Changes in concentrations of vitamin E in plasma, liver, or muscle, caused by the various treatments (other than vitamin E), were not related to protection against NMD or ED.
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PMID:Research note: efficacy of various flavonoids and simple phenolics in prevention of nutritional myopathy in the chick. 140 42

The effects of long-term vitamin E deficiency and supplementation on learning behaviour were investigated. Rats were fed vitamin E-deficient [VE(-)], -supplemented [VE(+)], or control standard food beginning after the age of 4 weeks. They were trained in an eight-arm radial maze learning task at the age of 17 months, and in a step-through passive avoidance response (PAR) task at the age of 25 months. In the radial maze task, both VE(-) and VE(+) animals required as many trials to reach the learning criterion as control animals. Scopolamine injection (0.25-0.5 mg/kg) after acquisition of the task decreased the number of correct choices dose-dependently; however, the degree of the drug effect on VE(-) and VE(+) rats did not differ from that on control rats. On the other hand, VE(-) animals showed significantly lower rate of avoidance response and VE(+) animals tended to show higher rate of avoidance response in the PAR task than did control animals. These results suggest that long-term vitamin E deficiency or supplementation does not influence general ability to acquire and maintain memory tasks in rats, but that it may affect learning behaviour, depending on the kind of task in which animals were trained.
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PMID:Learning behaviour in chronic vitamin E-deficient and -supplemented rats: radial arm maze learning and passive avoidance response. 146 82

Two children, aged 11 years, who originally had jejunal atresia corrected in the neonatal period, developed massive dilatation of the proximal small intestine. This resulted in circular muscular hypertrophy with lipofuscin deposits giving the typical appearance of "brown bowel." The condition was associated with malnutrition and vitamin E deficiency. Because of relatively short bowel, the condition was treated by limited resection and extensive tapering of the dilated segment, end-to-end reanastomosis, vitamin E supplementation, and intensive nutritional support.
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PMID:Brown bowel syndrome: a late complication of intestinal atresia. 146 88

It has been over 50 years since vitamin E was originally described as a lipid-soluble dietary constituent required for normal reproduction in rats. Vitamin E is recognized as an essential vitamin required for all classes of animals functioning predominantly as an intracellular antioxidant in maintaining the integrity of biological cell membranes. Although a wealth of information has been gathered on clinical signs of vitamin E deficiency, establishing its requirements for animals has been exceedingly difficult because of interrelationships with other dietary constituents. Vitamin E requirements for animals cannot be defined in isolation. Requirements are influenced by the amount and type of fat (particularly with monogastrics) and degree of fat oxidation in the diet; the presence of antioxidants; dietary selenium (closely interrelated with vitamin E), iron, copper, and sulphur amino acids, as well as the physiological status of the animal. Other factors to be considered in assessing vitamin E needs of animals under commercial production conditions include: a) variability of vitamin E content in feedstuffs; b) poor stability of vitamin E during processing and storage of feeds; and c) management practices resulting in overstressed animals. Information on the function of or requirements for vitamin E in animals is very incomplete. Estimated dietary vitamin E requirements for most animal species are in the range of 10-40 IU/kg of diet. Of particular concern is the lack of vitamin E requirement information regarding young dairy and beef calves. Although good experimental evidence indicates a beneficial role of supplemental vitamin E above physiological levels on overall performance, enhanced immunocompetence and preservation of meat and milk products, levels of vitamin E required to produce these desired effects needs to be firmly established. Present estimated dietary requirements for vitamin E across species may need to be redefined as new information becomes available about the role this nutrient plays in growth, health and overall metabolism.
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PMID:Comparative vitamin E requirements and metabolism in livestock. 147 5

The possible aggravation of liver injury by impaired cellular antioxidant function was investigated. A vitamin E-deficient diet (0.5 mg/kg alpha-tocopherol; control 100 mg/kg) significantly reduced rat liver alpha-tocopherol concentrations after 4 weeks (1.8 +/- 1.7 micrograms/g; control 34.4 +/- 2.4 micrograms/g, p < 0.001). The effects of copper loading (Cu, 3 g/kg diet); galactosamine (GalN, 0.85 g/kg i.p.); or carbon tetrachloride (CCl4, 10 mmol/kg i.p.) were examined. Serum aspartate transaminase activity was elevated slightly by vitamin E deficiency but not by hepatic copper accumulation. In vitamin E-replete (E+) and vitamin E-deficient (E-) rats, GalN or CCl4 caused a large and comparable elevation in serum AST and OCT activity. This effect on AST was markedly reduced by copper loading in vitamin E replete (E+) rats, but in E(-) rats copper had significantly less protective effect. Copper also diminished the OCT response to GalN in E+, though not E-, rats. A significant rise in total hepatic alpha-tocopherol content followed administration of GalN or CCl4 in both normocupric and copper-laden E(-) rats. Thus alpha-tocopherol deficiency (a) was not hepatotoxic per se; (b) failed to potentiate the toxicity of copper, GalN or CCL4; but (c) partially abolished the protection by copper against toxin-induced liver injury. Retention of hepatic alpha-tocopherol after liver damage may partly explain low serum vitamin E levels seen in clinical liver disease.
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PMID:Alpha-tocopherol deficiency fails to aggravate toxic liver injury but liver injury causes alpha-tocopherol retention. 148 10

Exercise induces free radical formation in muscle and liver, and oxidative damage, such as lipid peroxidation. The amount of damage depends on exercise intensity, training state and the tissue examined and can be reduced through dietary supplementation of antioxidants such as vitamin E and possibly coenzyme Q10. Supplementation with antioxidants does not increase maximal aerobic capacity or maximal exercise capacity; effects on endurance capacity are unclear. Deficiency of vitamin E or vitamin C greatly reduces endurance capacity, whereas selenium deficiency has no effect on endurance capacity. In studies by the authors, urinary output of the oxidatively damaged RNA base 8-hydroxyguanosine was not affected by several submaximal exercise bouts nor by supplementation with vitamins E and C and beta-carotene in moderately trained humans. In rats, endurance training caused an increase in oxidative damage, as measured by the protein carbonyl concentration of muscle, but not liver. Muscle protein carbonyl concentration returned to normal on detraining. These results indicate that the search for oxidative damage due to exercise and the effects of antioxidant manipulation on such damage should ideally involve examination of several indices of oxidative damage in various tissues after exercise and training.
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PMID:Exercise, oxidative damage and effects of antioxidant manipulation. 151 50

It is speculated that oxidative stress in vivo may have some influence on advanced, nonenzymatic, glycosylation end products. However, this has not been demonstrated yet. We assessed changes in collagen-linked fluorescence in the skin of nondiabetic and streptozotocin-induced diabetic rats fed three different diets for 4 weeks that could modify oxidative stress: vitamin E-deficient (D), vitamin E-supplemented (S), and control (C). The serum lipid peroxide level expressed as thiobarbituric acid (TBA) activity in diabetic rats on the S diet (9.6 +/- 1.0 [SE] nmol/L/mL) was significantly (P less than .01) lower than that in rats on the D diet (111.4 +/- 22.4), and similar to that in nondiabetic rats on the C diet (12.4 +/- 2.2). The collagen-linked fluorescence level was significantly (P less than .01) higher in diabetic rats than in nondiabetic rats, which corresponded to the serum glucose and glycosylated hemoglobin levels. However, there were no significant differences in the fluorescence levels among three groups classified by three different diets in both nondiabetic and diabetic rats (21.7 +/- 1.7 arbitrary U/mg collagen for D, 22.3 +/- 2.0 for C, and 22.8 +/- 2.5 for S in nondiabetic rats v 41.2 +/- 4.1 for D, 40.1 +/- 4.7 for C, and 39.3 +/- 3.5 for S in diabetic rats), despite significant changes in serum lipid peroxide levels. Consequently, there were no significant changes found in collagen-linked fluorescence levels in diabetic rats wherein oxidative stress was modified by vitamin E deficiency and supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No significant effect of vitamin E deficiency or supplementation on collagen-linked fluorescence in skin of diabetic rats. 151 18

Male Sprague-Dawley rats were fed from weaning low (1-5 ppm) and normal (26-50 ppm) vitamin E diets for 30-34 weeks. Dietary fat was also varied from 5% (Experiment 1) to 20% (Experiments 2 and 3). Intestinal tumors were induced by 1,2-dimethylhydrazine given subcutaneously as 10 weekly doses at 20 mg/kg body wt. Tumor incidence was lower by 30% and burden was 25%-50% lower for low vitamin E rats than for vitamin E-replete rats. This result was independent of the fat content of the diet. In Experiment 3, vitamin E and calcium were assessed for their influence on intestinal tumors at two levels, with dietary vitamin E at 5 and 50 ppm and calcium at 0.2% and 1.0% in a 2 x 2 factorial experiment. The high calcium-low vitamin E diet produced the greatest fall in tumor incidence and burden relative to the other treatments. In this experiment, vitamin E deficiency reduced tumor incidence and calcium supplementation reduced tumor burden, with a significant interaction of the two. However, this group also showed evidence of reduced food intake and kidney change (calcification), which may have confounded the result. This points to a risk associated with this combination of nutrients at these levels in long-term experiments.
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PMID:The influence of dietary vitamin E and calcium status on intestinal tumors in rats. 157 44

Experiments were carried out to measure the urinary excretion of free and conjugated malonaldehyde (MDA) and other thiobarbituric acid reactive substances (TBARS) in vitamin E deficient and vitamin E supplemented rats. From both dietary groups, six TBA positive fractions were isolated, in addition to that containing free MDA, by high-performance liquid chromatography (HPLC) on a TSK-GEL G-1000PW column. Three of the fractions isolated were found to be significantly increased in vitamin E deficiency. After acid hydrolysis, only one of the above compounds produced free MDA which indicated the presence of derivatized MDA. Only this fraction exhibited fluorescence at excitation 370 nm and emission 450 nm. The five other fractions formed 2,4-dinitrophenylhydrazones (2,4-DNPH), indicating the presence of carbonyl groups, but the derivatized MDA fraction did not. No significant differences were found in free MDA levels between the vitamin E deficient and the vitamin E supplemented groups.
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PMID:Urinary response to in vivo lipid peroxidation induced by vitamin E deficiency. 157 56


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