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

Weaning rats were divided into two groups, one group being fed a vitamin E-deficient diet, and the other an alpha-tocopherol-containing (50 mg/kg) control diet. Rats were killed at 1, 2, 3 and 4 months of feeding. The following results were obtained. 1. Both plasma and liver alpha-tocopherol levels decreased greatly by feeding vitamin E-deficient diet for 1 month, and thereafter decreased gradually by continued feeding. 2. Somehow different results were obtained concerning liver peroxidation value by the method of analysis. In the case of chemiluminescence, the value increased by vitamin E deficiency during the first 2 months, but thereafter, the value was almost unchanged. On the contrary, in the case of TBA-RS, the value increased gradually throughout the entire 4 months of feeding period. 3. Both plasma alpha-CPI level and pyruvate kinase activity increased by vitamin E deficiency, showing similar pattern of change with feeding period. Especially, marked increase of these values was observed in vitamin E-deficient rats fed for longer than 2 months, and differences from control groups were highly significant (in both cases, at 2 months, p < 0.005, and at 3 and 4 months, p < 0.001). And, in vitamin E-deficient group, including all the rats fed on test diet for 1 to 4 months, correlation between both values was very high, and was highly significant (r = 0.9060, p < 0.001).
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PMID:Correlation between plasma alpha-cysteine proteinase inhibitor level and pyruvate kinase activity in vitamin E-deficient rats. 129 45

The effects of vitamin E on toxicity by minute amounts of paraquat fed continuously for some period to rats were investigated. Two experiments were carried out as experiments 1 and 2. In both experiments, weaning rats were divided at first into two groups; one group was given a vitamin E-deficient diet, and the other a vitamin E-supplemented control diet (50 mg alpha-tocopherol/kg of diet). They were fed on these diets for 40 days. After that, in both experiments, the rats that had been fed the vitamin E-deficient diet were further divided into two groups, which were either given a paraquat-added diet (+PQ-E) or continuously fed the same vitamin E-deficient diet (-E). The amount of paraquat added was 250 mg of methyl viologen per kg of diet. After the addition of paraquat, these two groups were pair-fed. In experiment 1, paraquat was given to all the rats fed the vitamin E-supplemented control diet (+PQ+E). In experiment 2, rats fed the control diet were divided into paraquat-added (+PQ+E) and non-paraquat-added (+E) groups, similar to those of vitamin E-deficient rats. These two groups were also pair-fed thereafter. In both experiments, about 35 days after paraquat addition, they were sacrificed. Plasma and liver alpha-tocopherol contents were measured by HPLC, and liver peroxidation value was measured by chemiluminescence and the TBA method. And, as parameters of vitamin E deficiency, plasma pyruvate kinase and GOT activities and alpha-cysteine proteinase inhibitor (alpha-CPI) level were measured. When the analyzed values were compared between paraquat-added and the corresponding not-added control groups (+PQ-E vs. -E, +PQ+E vs. +E), the following results were obtained. In experiment 1, the values of plasma and liver alpha-tocopherol levels were significantly lower in the +PQ-E group than those of the -E group; however, liver peroxidation values and values of the three parameters of vitamin E deficiency were not different significantly. In experiment 2, the value of liver alpha-tocopherol level was significantly lower in the +PQ+E group than that of the +E group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of vitamin E on toxicity by minute amounts of paraquat fed continuously to rats. 188 Jun 28

The effects of dietary vitamin E and beta-carotene were studied on enzymes involved in arachidonic acid metabolism and other related enzymes in the rat testis. Groups of rats were fed various soybean oil-based semi purified diets. Group 1 was fed a vitamin E-supplemented diet (+E - beta); Group 2 was fed a beta-carotene-supplemented diet (-E + beta); Group 3, the control group (-E - beta) was fed a vitamin E-deficient diet; and Group 4, the standard diet group (S), was fed vitamin E plus beta-carotene-standard diet. Soybean oxidized oil was added to the three diet groups - (+E - beta), (- E + beta) and (- E - beta), whereas the diet of S group contained non-oxidized oil. After 8 weeks rats were killed, blood and testis samples were collected for biochemical determinations. Vitamin E deficiency caused significant increase in testis thiobarbituric acid value and activities of testis NADPH oxidase, testis 15-lipoxygenase and in plasma pyruvate kinase. In contrast, significant decreases were observed in activity of testis prostaglandin synthetase, compared with antioxidant-supplemented diet groups. We also found a significant increase in 15-lipoxygenase activity in (- E + beta) diet group, compared with (- E - beta) diet group. Fatty acid analysis of testis parenchyma indicated decrease in palmitate (16:0) and arachidonate (20:4(n - 6)), and increase in oleate (18:1(n-6)) linoleate (18:2(n - 6)) and linolenate (18:3(n - 3)), when compared (-E - beta) diet group with vitamin E-supplemented diet groups. The results suggest that dietary vitamin E has a role in both enzymatic and non-enzymatic peroxidation of polyunsaturated fatty acids in the testis.
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PMID:The effect of dietary vitamin E and beta-carotene on oxidation processes in the rat testis. 190 Dec 24

Liver disease, particularly alcoholic cirrhosis, is associated with a number of interesting chemical changes which result in structural and metabolic abnormalities of the erythrocyte membrane leading to microscopically observable cell shape changes and hemolytic anemia varying from very mild to potentially lethal. Increase in unesterified serum cholesterol owing to lecithin cholesterol acyl transferase (LCAT) deficiency in cirrhosis leads to expansion of the lipid bilayer and macrocytosis without megaloblastic changes in precursors. Substitutions of phosphatidyl choline (PC) moieties in the erythrocyte lipid bilayer lead to echinocytes (disaturated PC) or to stomatocytes (diunsaturated PC). In some patients, high density lipoprotein (HDL) abnormalities lead to erythrocyte surface changes causing rapid formation of echinocytes. The rapidity and reversibility of these changes suggest blockade of metabolic transport channels critical to the maintenance of erythrocyte membrane shape. Metabolic changes involving vitamin E deficiency leading to lipid peroxidation and pyruvate kinase instability leading to adenosine triphosphate (ATP) reduction have also been invoked to explain hemolysis associated with acute liver damage. The most severe hemolysis in liver disease is associated with acanthocytes (spur cells) and a marked imbalance in cholesterol-phospholipid ratio. These patients usually have hypersplenism, as well as rigid erythrocyte membrane transformations which are irreversible. Any of the other erythrocyte membrane shape changes described appear to be reversible if the liver disease abates, but they too may become irreversible if bits of projecting membrane are repeatedly removed by the macrophages of an enlarged spleen.
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PMID:Mechanisms of hemolysis in liver disease. 218 63

Weanling male Sprague Dawley rats were fed a vitamin E and C-free basal diet with or without supplementation of 100 IU vitamin E per kg diet. After 20 weeks, the vitamin E-deficient rats were divided into four groups, six in each group, and received supplemental ascorbic acid and/or vitamin E by tube feeding daily for 7 days: Group I, 30 mg ascorbic acid/100 g body wt.; Group II, 0.03 mg RRR-alpha-tocopheryl acetate/100 g body wt.; Group III, 30 mg ascorbic acid and 0.03 mg RRR-alpha-tocopheryl acetate/100 g body wt.; and Group IV, placebo. The six control rats (Group V) received placebo. The rats were sacrificed, blood and liver samples were collected for biochemical determinations. Vitamin E deficiency significantly increased erythrocyte (RBC) spontaneous hemolysis, liver thiobarbituric acid (TBA) value, activities of glutamateoxaloacetate transaminase (GOT), pyruvate kinase (PK), and creatine phosphokinase (CPK) in plasma, and significantly lowered plasma vitamin E levels and glutathione peroxidase (GPX) activities. Tube-feeding ascorbic acid for 7 days produced partial reversal effect on liver TBA values, activities of plasma PK, GOT, CPK, and plasma vitamin E levels but not on RBC hemolysis and plasma GPX activity. Tube feeding both ascorbic acid and vitamin E showed similar partial reversal effect as feeding vitamin E alone on all the parameters stated above. The results suggest that ascorbic acid may spare the metabolism of vitamin E and partially reverse the changes in some of the biochemical parameters characteristic of vitamin E deficiency.
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PMID:Effect of ascorbic acid and vitamin E on biochemical changes associated with vitamin E deficiency in rats. 344 Jul 14

Feeding a basal diet free of vitamins E and C to weanling male rats for 8 months resulted in biochemical changes characteristic of vitamin E deficiency. These included increased liver thiobarbituric acid values; decreased blood GSH levels, plasma vitamin E levels, and glutathione peroxidase activities; and increased activities of plasma pyruvate kinase, glutamic-oxaloacetic transaminase, creatine kinase, lactic dehydrogenase, and malic dehydrogenase. Tube-feeding vitamin C for 21 days resulted in partial reversal effects on the above parameters except activities of glutathione peroxidase, lactic dehydrogenase, and malic dehydrogenase. The results suggest that vitamin C may spare in part the metabolism of vitamin E through its antioxidant property.
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PMID:Vitamin C partially reversed some biochemical changes produced by vitamin E deficiency. 382 80

This study was designed to evaluate the effects of dietary vitamin E and synthetic antioxidants on prostacyclin (PGI2) synthesis in isolated aorta segments and perfused hearts as well as thromboxane (TxA2) synthesis in thrombin-stimulated washed platelets. Weanling male New Zealand rabbits were fed a vitamin E-deficient basal diet or the basal diet supplemented with either all-rac-alpha-tocopherol acetate or propyl gallate or DPPD (N,N'-diphenyl-p-phenylenediamine). After 30 days on the diet, plasma tocopherol level, pyruvate kinase and liver microsomal NADPH oxidase were determined. DPPD but not propyl gallate prevented the development of myopathy. None of the synthetic antioxidants could substitute for vitamin E in decreasing enzymatic lipid peroxidation. PGI2 release by the aorta was lowered in vitamin E deficiency and was highest with DPPD supplementation. In the Langendorff perfused heart, however, PGI2 release was highest in the vitamin E-deficient group, possibly due to cardiomyopathy. TxA2 synthesis by washed platelets challenged with thrombin was independent of the antioxidant status of the animal. The data showed that dietary antioxidants selectively affect eicosanoid synthesis in different tissues.
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PMID:Differential effects of dietary vitamin E and antioxidants on eicosanoid synthesis in young rabbits. 633 92

Weanling rats were fed either a vitamin E-deficient diet or the deficient diet supplemented with vitamin E or the antioxidant ethoxyquin. Ethoxyquin was not effective in preventing the elevation in platelet number or percent aggregation. However, ethoxyquin was as effective as vitamin E in maintaining body weight, testes weight, pigmentation of the incisors and in preventing myopathy, observed either histologically or by an elevation in plasma glutamic oxalacetic transaminase (GOT) activity. Removal of ethoxyquin from the diet after 19 weeks of feeding resulted in a rapid onset of myopathy. These observations permitted us to study the requirement for vitamin E at various ages without the complication of any cumulative pathological effects of vitamin E deficiency. Ethoxyquin was deleted from the diet at 8, 20, 44 and 64 weeks of age. The requirement for vitamin E to reduce plasma GOT and pyruvate kinase (PK) activity was measured at 12, 24, 48 and 68 weeks of age. The requirement for vitamin E did not change significantly during this time period.
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PMID:Influence of age on the vitamin E requirement for resolution of necrotizing myopathy. 738 1

Three series of experiments demonstrated that sesame seed and its lignans cause significant elevation of alpha-tocopherol content in rats. In Experiment 1, 20% sesame seed (with a negligible amount of alpha-tocopherol) supplementing 10 (low), 50 (normal), or 250 (high) mg/kg alpha-tocopherol diets (protein and fat concentrations in diets were adjusted to 200 and 110 g/kg, respectively) all caused a significant increase of alpha-tocopherol in the blood and tissue of rats. In Experiment 2, groups of rats were fed five different diets: a vitamin E-free control diet, a low alpha-tocopherol diet, and three low alpha-tocopherol diets supplemented with 5, 10, and 15% sesame seed. Changes in lipid peroxides in liver, red blood cell hemolysis, and pyruvate kinase activity, as indices of vitamin E deficiency, were examined. These indices were high in the low alpha-tocopherol diet, whereas supplementation with even 5% sesame seed suppressed these indices completely and caused a significant increase of alpha-tocopherol content in the plasma and liver. In Experiment 3, two diets containing sesame lignan (sesaminol or sesamin) and low alpha-tocopherol were tested. Results in both of the sesame lignan-fed groups were comparable to those observed in the sesame seed-fed groups as shown in Experiment 2. These experiments indicate that sesame seed lignans enhance vitamin E activity in rats fed a low alpha-tocopherol diet and cause a marked increase in alpha-tocopherol concentration in the blood and tissue of rats fed an alpha-tocopherol-containing diet with sesame seed or its lignans.
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PMID:Sesame seed and its lignans produce marked enhancement of vitamin E activity in rats fed a low alpha-tocopherol diet. 856 30

To study how the expression of alpha-tocopherol transfer protein (alpha-TTP) and its mRNA are affected by protein and vitamin E status, Long-Evans male weanling rats were fed a vitamin E-deficient (DE), high vitamin E (HE, 5 g/kg diet of all-rac-alpha-tocopheryl acetate) or control (C) diet for 12 wk in Experiment 1; and fed a low-protein (LP) or control (C) diet for 6 wk in Experiment 2. The high and deficient vitamin E status of HE and DE groups in Experiment 1 were confirmed by changes in plasma pyruvate kinase activity as well as the concentrations of alpha-tocopherol in plasma and liver. As shown by the Northern and Western Blot Analysis, the expression of alpha-TTP in the liver of the DE group was significantly lower than, while that of the HE group was not different from, that of the controls. In contrast, the alpha-TTP mRNA levels did not differ among the C, DE and HE groups. alpha-Tocopherol in most peripheral tissues of rats fed the LP diet in Experiment 2 was significantly lower than that of the C. Both the alpha-TTP and its mRNA were significantly lower in the LP group than in the C. The results suggested that dietary vitamin E does not affect alpha-TTP gene expression except that the protein levels in the liver were lowered by vitamin E deficiency. On the other hand, protein inadequacy appeared to down-regulate the expression of the alpha-TTP gene.
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PMID:Liver alpha-tocopherol transfer protein and its mRNA are differentially altered by dietary vitamin E deficiency and protein insufficiency in rats. 986 80


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