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

Xanthine oxidase which increases in activity during vitamin E deficiency was purified from livers of deficient rabbits. The procedure incorporates preparative sucrose gradient centrifugation and yields a homogeneous preparation on acrylamide gel electrophoresis. The purified enzyme exhibits a pH optimum of 8.1 and a Km value of 22 muM. Gel filtration chromatography gave the molecular weight of 280 000. Acrylamide gel electrophoresis in the presence of sodium dodecylsulphate reveals two types of subunits of molecular weights 52 000 and 99 000.
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PMID:Purification and characterization of xanthine oxidase from livers of vitamin E deficient rabbits. 23 93

An experiment was conducted to study the effects of feeding a 96.8% cull pea basal ration, low in selenium (0.061 ppm) and vitamin E (7.0 IU alpha-tocopherol/kg of ration), to growing pigs with and without supplementation of selenium, vitamin E, or both. The basal ration was high in crude protein (25.2%) and contained no supplemented fat. Nine of 10 pigs fed the unsupplemented basal ration had lesions attributed to selenium-vitamin E deficiency, and 8 of these pigs died during the 160-day experiment. The deficiency was usually characterized by sudden death (with no prior signs of illness), massive hepatic necrosis, hemoglobinuric and to a lesser extent cholemic nephrosis, degenerative myopathy of cardiac and skeletal muscles, edema, icterus, and acute terminal congestion and hemorrhage. Clinical signs, deaths, or lesions attributed to selenium-vitamin E deficiency were not observed in any of the pigs fed the basal ration supplemented with as little as 0.01 ppm selenium as sodium selenite or 100 ppm alpha-tocopherol. Pigs fed the unsupplemented basal ration gained more slowly (P less than 0.01) and less efficiently and had higher serum glutamic oxalacetic transaminase (SGOT) levels (P less than 0.01) than pigs fed the basal ration supplemented with selenium, vitamin E, or both. There was no difference (P greater than 0.05) in albumin-to-globulin (A/G) ratios among dietary treatment groups. Using the criteria of this study, the minimum selenium requirement of growing pigs fed a low tocopherol cull pea diet was determined to be between 0.06 and 0.07 ppm.
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PMID:Selenium-vitamin E deficiency in swine fed peas (Pisum sativum). 111 25

Vitamin E deficiency is a common consequence of chronic cholestatic liver disorders. Inasmuch as vitamin E content of cellular membranes alters membrane properties such as fluidity and molecular order, we postulated that vitamin E status could affect hepatocyte transport processes dependent on membrane integrity. Hepatocytes were isolated from rats maintained on diets containing deficient, sufficient, or excess vitamin E. Cell viability and oxygen consumption were maintained in all groups of hepatocytes. Hepatocyte uptake of taurocholic acid and ouabain and Na+,K(+)-ATPase activity estimated by rubidium-86 influx did not differ with vitamin E status. Vitamin-E-deficient hepatocytes had increased generation of lipid peroxide products. We conclude that deficient or excess vitamin E status had little effect on selected transport processes in normal hepatocytes.
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PMID:Effect of vitamin E on transport processes in isolated rat hepatocytes. 239 66

Female rats deprived of dietary vitamin E for 35 wk postweaning were analyzed for changes in vascular function. A functional state of vitamin E deficiency was indicated by a marked increase in spontaneous hemolysis of washed red cells by 22 wk of feeding. Elevated thiobarbituric acid-reactive material in aorta, liver, and plasma samples from vitamin-E deficient rats indicated increased lipid hydroperoxide formation. Systolic blood pressures and heart rates measured biweekly were unaltered by diet. Before being killed, the rats were catheterized and allowed to recover from anesthesia (methohexital sodium ip). The pressor response to graded doses of angiotensin II was significantly increased in the vitamin E-deficient group relative to its control. Isolated superior mesenteric artery segments from vitamin E-deficient rats demonstrated significantly decreased relaxation responses to acetylcholine. In contrast, artery contractile responses to 50 mM potassium and to graded doses of extracellular calcium did not differ, indicating that contractile capability was maintained. Surface blebbing of the femoral artery endothelium was observed by scanning electron microscopy. These data support a proposed link between lipid peroxidation and development of altered vascular function.
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PMID:Lipid peroxidation and altered vascular function in vitamin E-deficient rats. 273 27

Glutathione peroxidase activity in platelets increased stepwise in selenium-depleted rats that were repleted with graded levels of dietary sodium selenite. In a 3-phase depletion/repletion/depletion feeding study, glutathione peroxidase activity was similar in platelets and liver, which apparently contains the largest labile pool of selenium in the body. The activity of glutathione S-transferase (selenium-independent glutathione peroxidase) in platelets was low and was not affected by selenium deficiency, even though hepatic transferase was markedly elevated in selenium-deficient rats. Vitamin E deficiency did not affect activities of glutathione peroxidase or glutathione S-transferase in platelets or liver. Determination of glutathione peroxidase activity in platelets apparently is a promising technique for assessing selenium status and, possibly, for measuring selenium bioavailability.
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PMID:Platelet glutathione peroxidase activity as an index of selenium status in rats. 682 91

Vitamin E is known to play a protective role for cell membranes against free-radical attacks. Vitamin E deficiency causes a rapid macroscopic ageing of rats. On the other hand, during normal ageing, cell membranes undergo functional alterations resulting in an increased intracellular potassium concentration in brain and liver cells. Therefore, is was of interest to study whether vitamin E deficiency produces similar alterations in young rats. Female Wistar rats were fed with a vitamin E deficient diet from 1 month of age for 10 months. The parietal brain cortex and the liver were analyzed by means of a quantitative energy dispersive X-ray microanalytic method using a JEOL JSM-35C-EDAX-711-NOVA-3 system. Monovalent electrolyte contents as well as the water content of the cells were determined in 5 treated and 5 control animals. Water content was measured by analyzing the potassium content in aqueous, frozen state, and again in the dry mass of the cells. On the basis of these data, a computer program calculated the water proportions. Average values for 200 or more cells of each organ per group revealed a significant increase in the intracellular potassium content of the brain cells, whereas the sodium and chloride contents increased to a much lower extent. There was a 2.6% loss of intracellular water in the brain cells in the vitamin E deficient group. The liver monovalent ions and water content remained unchanged. The results obtained are discussed in terms of the membrane hypothesis of ageing.
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PMID:In vivo effects of vitamin E deficiency on the intracellular monovalent electrolyte concentrations in brain and liver of rat. An energy dispersive X-ray microanalytic study. 726 78

Lungs accumulate 5-hydroxytryptamine (serotonin, 5-HT) from the perfusate by a sodium-dependent, energy-requiring, saturable process. The rate-limiting step for uptake is the transport of 5-HT and not its subsequent metabolism to 5-hydroxyindoleacetic acid. Autoradiographic studies indicate that the pulmonary endothelium is the cellular site of uptake. The effect of hyperoxia on lung clearance of 5-HT was studied with isolated perfused and ventilated lungs from rats that were previously exposed to hyperoxia. Lungs were perfused with recirculating electrolyte solution and initial [5-HT] of 0.24 microM. The calculated fractional 5-HT clearance (fracion of 5-HT removed in a single pass) ws 0.77 +/- 0.02 (mean +/- SE: n = 44) for control rats. Mean fractional clearance decreased by 20% in rats exposed to 1 atm O2 for 18 hr and 30% after 4 atmospheres absolute (ata) O2 for 1 hr (p < 0.05). The effects of O2 at 4 ata were in part reversed by exposure to air for 3.5 hr and in part prevented by injection of superoxide dismutase (60 nmole/kg body weight). This degree of O2 exposure at either 1 or 4 ata had no effect on lung content of adenine nucleotides or the distribution of 3H-5HT on autoradiography. Rats maintained for 6 weeks on a vitamin E-deficient diet showed an increased effect of hyperoxia on 5-HT clearance and did not show reversal of changes after 24 hr of air breathing. The results indicate that exposure to elevatd po2 results in reversible depression of pulmonary 5-HT clearance that is potentiated by vitamin E deficiency. This suggests alteration of pulmonary endothelial membrane transport properties due to O2 toxicity.
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PMID:Environmental influences on uptake of serotonin and other amines. 740 97

1. The effects of vitamin E deficiency were evaluated in aortic rings isolated from rats maintained on a diet deficient in vitamin E. 2. Endothelium-dependent vasodilator responses to acetylcholine (ACh) and calcium ionophore, A23187, were reduced in preparations from treated animals, compared to the age-matched controls. The maximal vasodilation to ACh was 66.4 +/- 9 (n = 4) and 38.8 +/- 7 (n = 4) % in control and 10 month-treated preparations, respectively. 3. The endothelium-independent vasodilator responses to sodium nitroprusside as well as the concentration-dependent contractile responses to noradrenaline, did not differ between treated and control preparations. 4. Electron microscopic examination of vascular segments and revealed that, following vitamin E deficiency, normal tissue organisation was disrupted, the endothelial monolayer either not being in contact with the underlying tissue or being absent in most of the areas analysed. 5. It is concluded that during vitamin E deficiency both morphological disruption and functional impairment of endothelium occur without observable modification of muscle cell function and morphology.
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PMID:Effects of vitamin E deficiency on vasomotor activity and ultrastructural organisation of rat thoracic aorta. 758 51

1. Thoracic aortae, isolated from rats supplemented with dietary vitamin E after vitamin E deficiency, were analysed for changes in vascular reactivity. 2. Following 4 or 12 months of dietary vitamin E deficiency, endothelium-dependent vasodilator responses to acetylcholine were significantly impaired. However, when animals were fed after the first 4 months of vitamin E deprivation with a vitamin E-supplemented diet for 8 months, endothelium-mediated responses were completely restored. 3. In contrast, the endothelium-independent vasodilator or vasoconstrictor responses to sodium nitroprusside and noradrenaline, respectively were not altered either by vitamin E deficiency or supplementation. 4. These data indicate that vitamin E supplementation reversed the impairment of endothelial cell function which occurs during vitamin E deficiency.
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PMID:Recovery after dietary vitamin E supplementation of impaired endothelial function in vitamin E-deficient rats. 807 70

1. A vicious cycle of malabsorption and malnutrition has been implicated in the pathogenesis of protracted diarrhoeal disease in infancy. Vitamin E deficiency is common in malnourished infants with protracted diarrhoea. We have studied the effects of chronic vitamin E deficiency on small-intestinal secretion and absorption in the rat. 2. Weanling rats were fed vitamin E-sufficient or -deficient diets for 21 weeks. Jejunal function was studied in vitro in an Ussing chamber after this period. 3. Steady-state isotopic flux experiments in unstimulated tissues demonstrated net Na+ and Cl- secretion in vitamin E-deficient jejuna but net Na+ and Cl- absorption in vitamin E-sufficient jejuna. 4. Basal intestinal short-circuit current was the same in both groups. 5. Cyclic nucleotide and maximal non-neuronal acetylcholine-mediated electrogenic secretion were increased in vitamin E-deficient jejuna. 6. Exogenous 5-hydroxytryptamine (serotonin) induced a smaller increment in electrogenic secretion in vitamin E-deficient jejuna. 7. Vitamin E-deficient jejuna were less responsive to exogenous noradrenaline, resulting in a smaller alpha 2-adrenergic-mediated decrease in intestinal short-circuit current. 8. Fasting for 72h produced a greater increment in intestinal short-circuit current in vitamin E-deficient jejuna. 9. Chronic vitamin E deficiency is prosecretory in the small intestine and may predispose to the perpetuation of protracted diarrhoeal diseases.
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PMID:Modulation of small-intestinal secretion and absorption in chronic vitamin E deficiency: studies in rat jejunum in vitro. 828 52


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