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

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

In summary, we propose the following scheme (Figure 5) to describe the role of peroxidation in the pathophysiology of SCA. Sickle erythrocytes are more susceptible to peroxidation than are normal erythrocytes. This increased susceptibility to peroxidation is, in part, due to decreased blood vitamin E levels and abnormal membrane phospholipid organization induced by sickling. The peroxidative damage of sickle erythrocytes may accelerate or contribute to loss of cell deformability and to chronic hemolysis. Peroxidative damage can produce abnormal cellular properties, such as potassium leak and reduced filterability, and contribute to formation of ISCs. Increased red cell rigidity can initiate episodes of capillary obstruction, leading to vasoocclusive painful crises and to tissue infarction. Liver dysfunction as well as increased production of bilirubin secondary to hemolysis could result in bile sludging and decreased secretion of bile salts into the intestinal lumen. Reduced bile salt secretion leads to partial fat and vitamin E malabsorption. Vitamin E deficiency enhances red cell susceptibility to peroxidation and promotes a vicious cycle in SCA. Although we have not studied factors that might initiate peroxidative damage, sickle hemoglobin and excess body iron should be considered as potential sources. Our studies suggest that vitamin E supplementation to sickle-cell patients could be of clinical benefit.
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PMID:Peroxidation, vitamin E, and sickle-cell anemia. 695 61

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

1. Male rats were deprived as weanlings of dietary vitamin E and fed on a high polyunsaturated fatty acid (PUFA) diet for 6 months. Rats fed on a high PUFA or on an untreated diet served as controls. Mesenteric arterial beds were isolated and perfused at a constant flow rate (5 ml min-1) and the function of sympathetic nerves, smooth muscle and endothelium was assessed. 2. Electrical field stimulation (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent vasoconstriction of the mesenteric arterial preparations. Response curves were similar between untreated control and PUFA-fed control groups. Maximum vasoconstrictor responses (at 24 and 32 Hz) were significantly attenuated in rats deprived of vitamin E and on a high PUFA diet compared to the PUFA-fed controls (P < 0.05). 3. Exogenous noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent constriction of the mesenteric arterial beds. Preparations from rats fed on a high PUFA diet elicited significantly smaller responses compared to the control group. There was no significant difference in constrictor responses of PUFA rats deprived of vitamin E compared to the PUFA controls. Vasoconstrictor responses to doses of adenosine 5'-triphosphate (ATP) (5-5000 nmol) were significantly impaired in vitamin E-deficiency with a high PUFA diet compared to a high PUFA diet alone (P < < 0.001). Constrictor responses to potassium chloride (0.15 mmol) were significantly impaired in vitamin E-deficient PUFA rats compared to the PUFA-fed control group (P < 0.05). 4. Vasodilator responses were assessed in preparations in which tone was raised by continuous perfusion with methoxamine (4-25 microM). Mesenteric arterial beds from PUFA-fed rats deprived of vitamin E acquired significantly less tone, 59.8 +/- 4.6 mmHg (n = 7), than PUFA-fed controls 116.9 +/- 7.6 mmHg (n = 7) (P < 0.001) and were refractory to further increases in tone with further additions of methoxamine. Methoxamine-induced tone of PUFA-fed controls was greater than in P that in the untreated controls (83.9 +/- 7.4 mmHg; n = 5) (P < 0.05). Responses to the endothelium-dependent vasodilators acetylcholine (ACh) and ATP were significantly reduced in preparations from rats fed on the vitamin E-deficient high-PUFA diet compared to PUFA controls. Vasodilator responses to ACh were greater in PUFA controls than in untreated controls and this reached statistical significance at 5 nmol ACh. 5. Vasodilator responses to sodium nitroprusside, which acts directly on the vascular smooth muscle, were similar in untreated control and PUFA control groups. Responses were significantly attenuated in vitamin E-deficient PUFA rats compared to the PUFA control group (P < < 0.001). 6. These results indicate that a combination of a high PUFA diet and vitamin E deficiency impairs mesenteric arterial function at the level of the vascular smooth muscle. A high PUFA diet alone attenuates responses to NA and augments endothelium-dependent vasodilation. The detrimental effects of loss of antioxidant activity due to vitamin E-deficiency on vascular function may be exacerbated by a high PUFA diet.
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PMID:Effects of chronic vitamin E deficiency and a high polyunsaturated fatty acid diet on rat mesenteric arterial function. 868 Jul 46

Marked electrolyte abnormalities characterized by profound hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia were noted in 4 neonatal foals with acute rhabdomyolysis and pigmenturia. In 2 foals, rhabdomyolysis developed 4-6 days after admission for dysmaturity, and in 2 foals, rhabdomyolysis was evident on presentation. Rhabdomyolysis was a consequence of selenium deficiency with or without vitamin E deficiency, possibly combined with increased oxidant stress due to sepsis or hypoxia and reperfusion injury after parturition. Foals gained from 7 to 15% of their initial body weight within 48 hours of developing rhabdomyolysis. Three of the foals developed cardiac arrhythmias characterized by spiked T waves and decreased-amplitude P waves. Postmortem examination of 2 foals revealed extensive myodegeneration and renal tubular nephrosis; renal cortical necrosis with myocardial necrosis was noted in 1 foal. Destruction of the major intracellular compartment (intracellular fluid [ICF]) through extensive myonecrosis combined, in some cases, with myoglobinuric renal insufficiency produced major fluid shifts and life-threatening electrolyte derangements. With the major ICF compartment disrupted, hyperkalemia was most effectively treated using mineralocorticoids, loop diuretics, and ion exchange resins to enhance elimination. In addition, i.v. calcium, glucose, insulin, and sodium bicarbonate were administered, which helped redistribute potassium to the ICF. Severe rhabdomyolysis should be included in the differential diagnoses of hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia in neonatal foals.
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PMID:Electrolyte disturbances in foals with severe rhabdomyolysis. 959 79

Substances possessing the same histochemical properties as the ceroid in cirrhotic livers of rats fed choline-deficient diets have been prepared from various unsaturated fats, fatty acids and their esters by autoxidation but could not be obtained from hydrocarbons or saturated fats or fatty acids. The formation of ceroid-like substances occurred first on surfaces or at interfaces in the reaction mixtures. It was inhibited by antioxidants and was accelerated by the addition of tissues, blood cells, erythrocytic stroma, or hemoglobin, by emulsification, by increasing the surface exposed to the air, and by increasing the temperature. Histochemical studies provided much evidence that the following properties of ceroid might be attributed to the products of the autoxidation of unsaturated lipids: insolubility in organic solvents, sudanophilia, yellowing by concentrated nitric acid, positive periodic acid-Schiff's reaction, basophilia, acid fastness, positive hernofuscin reaction, and reduction of diammine silver carbonate and alkaline potassium permanganate. The normal reactivity of cells or tissues embedded in ceroid was effectively masked by the pigment, apparently, initially at least, by preventing the reagents' gaining access to them. It is suggested that the iron sometimes demonstrated in ceroid may be that of blood cells or tissue fragments incompletely masked by the ceroid. It is concluded that whenever conditions are such that unsaturated fats accumulate in tissues to such an extent that a relative lack of biological anti-oxidants results, autoxidation of the fats and their conversion to ceroid pigment are favored, and that ceroid and the lipofuscin pigment of vitamin E deficiency may be fundamentally similar.
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PMID:The in vitro preparation and histochemical properties of substances resembling ceroid. 1489 99