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

The effect of oxygen (O2) exposure on the ability of the isolated, perfused rat lung to clear serotonin (5-hydroxytryptamine, 5-HT) from the perfusate was evaluated in normal or vitamin E-deficient Sprague-Dawley rats. Rats were exposed to 100% O2 at 1 ATA for 4-48 h. Lungs were subsequently isolated, artificially ventilated, and perfused in a recirculating system with Krebs-Ringer bicarbonate solution, pH 7.4 containing 3% bovine serum albumin and 0.25 muM [14C] 5-HT. 5HT clearance was calculated from the disappearance rate of [ 14C] 5-HT from the perfusate. In normal rats exposed to 100% O2, there was a progressive reduction in the clearance of 5-HT with increasing duration of O2 exposure. Compared to lungs from air-exposed controls, clearance was depressed 20% (P less than 0.01) after 18 h, 22% (P less than 0.01) after 24 h, and 35% (P less than 0.001) after 48 h. With vitamin E-deficient rats, the reduction in 5-HT clearance occurred after a shorter exposure time and was of greater magnitude than in rats on a normal diet. Depression of 5HT clearance by the lungs is an early alteration of lung function fue to hyperoxia and is potentiated by vitamin E deficiency. The most likely mechanism for the depression of 5-HT clearance is interference with the transport properties of lung endothelium.
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PMID:Depression of serotonin clearance by rat lungs during oxygen exposure. 83 74

Clearance of 5-hydroxytryptamine (5-HT) by the lungs of normal and vitamin E-deficient rats was evaluated following a 60-min exposure to 100% oxygen (O2) at 4 ATA (HBO). After exposure, lungs were isolated, ventilated, and perfused, with a recirculating system used for measurement of 5-HT clearance. Control lungs were obtained from rats exposed to air at 1 ATA. In control normal rats, fractional clearance of 5-HT was 0.78+/-0.03 (mean+/-SE). Following HBO 5-HT clearance was 0.55+/-0.04 (P less than 0.01). In control vitamin E-deficient rats. 5-HT clearance was 0.85+/-0.05 and was decreased to 0.46+/-0.03 (P less than 0.001) following HBO. To evaluate the effect of recovery time after HBO on 5-HT clearance, separate groups of rats were killed at varying intervals post-HBO. In normal rats, 5-HT clearance had returned to control levels by 3-4 after HBO; in vitamin E-deficient rats, clearance remained unchanged 4 h after HBO and was only 74% (P less than 0.001) of control values 24 h post-HBO. These results indicate that depression of pulmonary 5-HT clearance occurs in rats due to hyperoxia and is potentiated by vitamin E deficiency. This represents a reversible alteration of lung function which requires vitamin E for complete recovery.
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PMID:Effect of hyperbaric oxygen exposure on pulmonary clearance of 5-hydroxytryptamine. 89 79

Both brown fat tissue (BAT) and skeletal muscle experience large increases of oxygen consumption and oxygen radical generation during activation. This, together with the relatively low activities of antioxidant enzymes in these two tissues and the high lipid content and free fatty acid liberation of BAT, can produce a physiological oxidative stress. Increases of in vivo or in vitro (BAT) lipid peroxidation have been described in these tissues after activation. They react to this oxidative stress in an adaptive way after chronic stimulation. Cold acclimation increases antioxidant enzymes, ascorbate, and especially reduced glutathione (GSH) in BAT. There is controversy about the variations of antioxidants in skeletal muscle after acute exercise. Nevertheless, exercise training seems to increase muscle antioxidant enzymes and GSH. Many reports show that vitamin E levels decrease in the muscle and increase in plasma during exercise. Studies of vitamin E deficiency and supplementation strongly suggest that this vitamin is of protective value during exercise.
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PMID:Brown fat thermogenesis and exercise: two examples of physiological oxidative stress? 139 16

Age-related alterations in both antioxidant capacity and lipid peroxidation in the cerebrum, lung and liver homogenates of normal and vitamin E-deficient rats were investigated. The antioxidant capacity, which includes superoxide dismutase, catalase and glutathione peroxidase activities and vitamin E (alpha-tocopherol) concentration, was relatively stable throughout the lifespan. It was observed, however, that catalase and glutathione peroxidase activities in livers of old rats decreased and that vitamin E concentration in lung and liver increased with age. In vitamin E-deficient animals, catalase activity in liver increased and glutathione peroxidase activity in liver and lung decreased. Lipid peroxidation was monitored by use of three different indices, i.e. the thiobarbituric acid (TBA) value, oxygen absorption and conjugated-diene formation. In the absence of any initiator, neither oxygen absorption into tissue homogenates nor conjugated-diene formation in lipid extracts from the homogenates occurred. The TBA value of each cerebrum homogenate incubated under air or an oxygen atmosphere was larger than that of the corresponding unincubated cerebrum homogenate. From comparison between the TBA value and oxygen absorption, this increase in the TBA value was suggested to be due to some reactions other than lipid peroxidation. Although tissue homogenates examined contained TBA-reacting materials, no lipid peroxidation seems to arise during incubation of them. No age-related alterations in the TBA value and oxygen absorption in rat tissue homogenates were observed. Vitamin E deficiency had no effect on the TBA values of cerebrum and lung homogenates, while it seemed to increase the TBA values of liver homogenates. Vitamin E deficiency had no effect on oxygen absorption in these tissue homogenates. The induction period of initiator-induced conjugated-diene formation in lipid extracts from liver and lung homogenates from normal and vitamin E-deficient rats tended to be extended with age. Vitamin E deficiency decreased the induction period of initiator-induced conjugated-diene formation. As a result, the length of the induction period was found to be proportional to vitamin E concentration in lipid extracts. The overall antioxidant capacity of rat tissues appears to be maintained without large variation during ageing. Decreases in the capacity of some antioxidant factors may be compensated by increases in the capacity of other factors.
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PMID:Age-related alterations in antioxidant capacity and lipid peroxidation in brain, liver, and lung homogenates of normal and vitamin E-deficient rats. 140 85

Several intellectual "autopsies" have recently reviewed errors in clinical epidemiologic studies of causation, such as the original claim that amyl nitrite "poppers" caused AIDS. The current autopsy was done to determine why it took more than a decade--1942 to 1954--to end an iatrogenic epidemic in which high-dose oxygen therapy led to retrolental fibroplasia (RLF) in premature infants, blinding about 10,000 of them. The autopsy revealed a museum of diverse intellectual pathology. When first noted, RLF was regarded as neither a new disease nor a postnatal effect. In early investigations, the ophthalmologists did not establish explicit criteria for diagnosis and confused RLF with malformations previously seen in full-term infants. Because the patients were not referred until months after birth, the ophthalmologists assumed that the lesion, which resembled an embryologic structure, must have occurred prenatally. Other events suggesting a prenatal cause for RLF were its strong statistical associations with fetal anomalies, multiple gestations, and maternal infections. Although these events were also associated with prematurity, it was ignored when the RLF cases were compared with controls who were mainly full-term infants. The postnatal timing of RLF was eventually recognized when investigators did cohort studies in premature infants and found that RLF could develop in eyes that were normal at birth. As the search for a cause turned to events occurring after birth, statistical associations were produced for agents such as light, vitamins, iron, vitamin E deficiency, and hypoadrenalism. Each study had its own methodologic flaws: controls were missing for light; co-maneuvers were ignored for vitamins and iron; objective diagnosis was not used for vitamin E deficiency; and the research on hypoadrenalism contained biases in susceptibility and detection as well as problems of a competing outcome event. When the role of oxygen administration was first considered, the statistical association with RLF was stronger for vitamin- and iron-therapy than for oxygen. In addition, many investigators were dissuaded by contradictory evidence from institutions in which RLF was either absent despite high-dose oxygen or persistent despite reduced dosage. The contradictory evidence was later regarded as erroneous because of unsatisfactory delivery systems for the oxygen or failure to check the actual oxygen concentrations. An alternative explanatory hypothesis, rejecting the role of high-dose and long-duration oxygen, was the idea that RLF was due to "relative hypoxia", produced by overly rapid weaning from oxygen therapy rather than the duration of oxygen treatment itself.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxygen as a cause of blindness in premature infants: "autopsy" of a decade of errors in clinical epidemiologic research. 143 8

Nerve tissue (as well as capillaries and cerebral microvessels) has a very high concentration in polyunsaturated fatty acids belonging to linoleic and alpha-linolenic series. Nerve tissue also requires large amounts of oxygen. Radical peroxidation of the polyunsaturated fatty acids represents a serious risk to the biochemistry and physiology of the membranes: it can be a cause of cellular death. During aging, the capillaries and cerebral microvessels undergo extensive modifications at the level of the polyunsaturated fatty acids: for example, the concentration of arachidonic acid decreases by half. In brain in general, vitamin E is very well protected: after oxidation, it is rapidly regenerated; it seems to undergo only slight degradation. In case of dietary deficiency, the brain loses much less vitamin E, and at a slower rate, than other non-nerve tissue. During aging, there is a relation between the content in vitamin E and the concentration of polyunsaturated fatty acids of the linoleic series, but not of the alpha-linolenic series. In addition, vitamin E deficiency also leads to a decrease in the enzymatic activities that protect against peroxidation of fatty acids.
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PMID:[Vitamin E: protection of membrane polyunsaturated fatty acids against radical peroxidation in the course of cerebral aging, particularly in cerebral capillaries and microvessels]. 180

Even though vitamin E may not improve physical achievements in sports competitions, as shown in several swimming experiments, it is important for the health of skeletal muscle: in its role as the major lipid-soluble chainbreaking antioxidant in lipid cell membranes, vitamin E protects muscle tissue in aerobic exercise, in which oxygen metabolism and, consequently, free radical production are greatly accelerated. Animal studies in several laboratories have shown that endurance exercise results in the same type of oxidative muscle damage as does vitamin E deficiency: there is an increase in the peroxidation products pentane and malondialdehyde and in enzymes leaked from muscles to plasma. Oxidative tissue damage in vitamin-E deficient animals is exacerbated by endurance training and, conversely, it is reduced by high-dose vitamin E supplementation; also, preliminary studies in humans have demonstrated antioxidant protection by high-dose vitamin E supplementation. After endurance exercise leakage of enzymes into the plasma and output of pentane in the breath were significantly reduced. During a high-altitude expedition in the Himalayas, protection was shown to be significantly better in the supplemented group than in the placebo group, as determined by anaerobic threshold and pentane exhalation.
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PMID:Function of vitamin E in physical exercise: a review. 189 77

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

Lipoprotein secretion and vitamin E transport depend on an adequate supply of inositol which functions synergistically with choline. Feeding rats a choline deficient diet was associated with decreased linoleic and arachidonic acids and increased docosapentenoic and docosahexenoic acids in liver phosphatidylethanolamine. Lipoprotein secretion by the liver is impaired by long chain omega 3 fatty acids and by the high carbohydrate diet of Kwashiorkor. Pulmonary surfactant is a lipoprotein which functions in preventing alveolar collapse in the lung. Inositol supplements to premature infants altered the composition of surfactant phospholipids and reduced the need for oxygen therapy. Oxygen free radicals, generated in oxygen therapy, convert low density lipoproteins (LDL) into potent toxins, without adequate antioxidants and free radical scavengers to block free radical generation. Vitamin E deficiency predisposes humans to increased susceptability to oxygen toxicity leading to Bronchopulmonary dysplasia (BPD), a form of chronic pulmonary insufficiency.
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PMID:Sudden infant death syndrome and lipoproteins. 266 28

The effects of dietary vitamin E deficiency on mouse cerebral membrane order and oxygen reactive species were studied. Quantitation of vitamin E levels in several brain regions showed greatest deficiencies in striatum and cerebellum, followed by substantia nigra, and cortex. Vitamin E deficiency increased central-core membrane order in cerebral P2 fraction, but was without effect in the superficial hydrophilic membrane domain. Oxygen radical formation was studied using the probe 2',7'-dichlorofluorescein diacetate. Basal generation rates of oxygen reactive species were 2.5-fold higher when compared to control animals. While hepatic levels of vitamin E are much more reduced than brain levels, in deficient mice, the rate of oxygen radical formation in the liver was unaltered. This implies an special susceptibility of the brain to deficiency of this lipophilic antioxidant vitamin. Data demonstrate that endogenous levels of free radical scavengers, such as vitamin E, may play an important role in maintaining basal oxygen radical levels and membrane integrity. The dietary vitamin E depletion paradigm suggests that a relation exists between elevated levels of oxygen radicals and more rigid hydrophobic central-cores in cerebral membranes, effects that may play a role in mechanisms underlying the neuropathologic lesions observed following vitamin E deficiency.
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PMID:Perturbations in cerebral oxygen radical formation and membrane order following vitamin E deficiency. 278 27


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