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

One hundred and twenty female mice fed diets containing various levels of vitamin E were continuously exposed to 0.5 ppm, 1.0 ppm nitrogen dioxide (NO2), and filtered air for 17 months. Blood, lung, and liver tissues were assayed for glutathione peroxidase (GSH-peroxidase) activity. Exposure to 0.5 ppm NO2 did not affect blood and lung GSH-peroxidase activity; 1.0 ppm NO2 exposure, however, caused suppression of the enzyme. A combination of vitamin E deficiency and 1.0 ppm NO2 exposure resulted in the lowest GSH-peroxidase activities in the blood and lung. High levels of vitamin E in the diet resulted in elevated GSH-peroxidase in the blood and lung. Liver GSH-peroxidase activity was unaffected by either dietary vitamin E or NO2 exposure. No inverse relationship was found between GSH-peroxidase levels and concentrations of organic solvent soluble lipofuscin pigments present in tissues.
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PMID:Long-term NO2 exposure of mice in the presence and absence of vitamin E. II. Effect of glutathione peroxidase. 73 11

The influence of dietary peroxides, vitamin E and selenium on glutathione peroxidase (GSH-Px) activity in the gastrointestinal tract of the rat was investigated. Feeding 7% oxidized stripped corn oid (peroxide value 1,000) in a diet adequate in selenium and vitamin E increased the specific activity of GSH-Px in the stomach mucosa. Feeding oxidized oil produced an increase in the wet weight of the intestinal mucosa which was associated with a decrease in the specific activity of the enzyme. Total GSH-Px activity in the intestinal mucosa was unchanged or moderately increased. These changes were unaffected by the presence of vitamin E in the diet. Dietary peroxides had no effect on GSH-Px activity in the plasma or in the perirenal and paraepididymal adipose tissues. Subacute vitamin E deficiency had no consistent effect on the activity of the enzyme in several tissues examined. In rats fed a Se deficient diet glutathione peroxidase activity decreased markedly in most tissues but only slightly in the intestinal mucosa. The moderate decrease in the intestine may be explained by the accessibility of residual dietary Se to the mucosal cells. The role of Se in the detoxification of peroxides in foods and the response of gastrointestinal GSH-Px to dietary peroxides are discussed.
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PMID:Influence of dietary peroxides, selenium and vitamin E on glutathione peroxidase of the gastrointestinal tract. 126 68

Vitamin E and selenium (Se) interact synergistically as an important antioxidant defense mechanisms. Se, an essential component of glutathione peroxidase (GSH-Px) and vitamin E decompose fatty acid hydroperoxides and hydrogen peroxides generated by free radical reactions. Vitamin E and GSH-Px may modulate arachidonic acid metabolism and the activity of cyclooxygenase enzymes by affecting peroxide concentration. The balance between arterial wall prostacyclin (PGI2) production and platelet thromboxane (TX)A2 directly influences platelet activity. In order to elucidate the differential role of dietary vitamin E and Se in aortic PGI2 and platelet TXA2 synthesis, 1-mo-old F344 rats were fed semipurified diets containing different levels of vitamin E (0, 30, 200 ppm) and Se (0, 0.1, 0.2 ppm) for 2 mo. Thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, were measured by radioimmunoassay (RIA) after incubation of whole blood and aortic rings at 37 degrees C for 10 and 30 min, respectively. Vitamin E deficiency reduced plasma vitamin E to 5-17% of control-fed rats, and supplementation in vitamin E-supplemented animals increased plasma GSH-Px by 17%, compared to vitamin E-deficient rats. Se and vitamin E supplementation did not have a similar effect on TXB2 and PGI2 synthesis. Se deficiency did not alter platelet TXB2 synthesis, but significantly decreased aortic PGI2 synthesis. It was necessary to supplement with both antioxidants in order to increase PGI2 synthesis. Se and vitamin E deficient groups had a higher TXB2/PGI2 ratio (0.17 +/- 0.08) compared to Se- and vitamin E-supplemented groups (0.03 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E. 137 63

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

Selenium deficiency is responsible for Zenker type muscle degeneration in calves, lambs, and foals in the prenatal and postnatal stages of development. Investigations have shown that the selenium GSH Px, and vitamin E content of the maternal and fetal parts of the placenta in cattle are different. Similarly, low concentrations of selenium are present in milk from cows and sheep. In addition to an inadequate supply of selenium and vitamin E as a contributory cause of fetal nutritive muscular dystrophy (FNMD), it is assumed that a placental transport block and/or impaired selenium metabolism in the placenta are also responsible. Postnatal nutritive muscular dystrophy, however, is attributed to either acute selenium and vitamin E deficiency in basic feed or impaired plant absorption of selenium as a result of antagonistic elements, such as sulphur.
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PMID:The importance of selenium in the prenatal and postnatal development of calves and lambs. 170 68

Four-week-old Wistar male rats were fed a vitamin E (VE)-deficient (0E) or a VE-sufficient (10E) diet for 6 weeks and then intraperitoneally treated with buthionine sulfoximine (BSO) at 1 mmol/kg body weight once a day for 3 days. Glutathione (GSH) depletion by BSO treatment caused injuries especially in the kidneys of VE-deficient rats. The kidney weight increased in the VE-deficient rats after BSO treatment (0E-BSO). It was observed that the epithelial cells of the renal tubules in this group were strongly impaired and the injuries were necrosis and desquamation. No injury was observed in the kidneys of the BSO-untreated 0E group and the 10E groups. The TBA value of the kidney of 0E-BSO group was lower than that of the BSO-untreated 0E group, but the lipofuscin content of the kidney of the 0E-BSO group was 10 times higher than that of the BSO-untreated 0E group. These results suggest that the kidney injuries in rats may be caused by lipid peroxidation induced by vitamin E deficiency and glutathione depletion.
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PMID:Kidney injury induced by lipid peroxide produced by vitamin E deficiency and GSH depletion in rats. 188 Jun 35

Vitamin E and glutathione protect against oxidative damage in vivo. In this study the relationship between these two defenses has been examined in the isolated perfused rat liver. The activities of glutathione reductase and glutathione S-transferase were unaffected by vitamin E deficiency, while glutathione peroxidase activity was decreased slightly. The glutathione redox status of vitamin E-deficient and control livers was assessed. GSSG was slightly higher in vitamin E-deficient livers (70 +/- 5 nmol GSH equivalents/g liver) than in controls (56 +/- 3 nmol GSH equivalents/g liver) under basal conditions. However, biliary GSSG release was 41% lower in vitamin E-deficient livers (0.46 +/- 0.08 nmol GSH equivalents/g liver.min) than in controls (0.78 +/- 0.23 nmol GSH equivalents/g liver.min). Inhibition of GSSG reduction by BCNU raised liver and biliary GSSG by a similar amount in vitamin E-deficient and control livers. Thus biliary GSSG efflux, a frequently used index of oxidant stress, is not increased in vitamin E-deficient perfused livers compared with control. Therefore, in the perfused rat liver model, no evidence was obtained that vitamin E deficiency activates the hepatic glutathione system.
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PMID:Tissue and biliary glutathione disulfide in the perfused vitamin E-deficient rat liver. 272 89

Selenium deficiency for periods of 5 or 6 weeks in rats produced an inhibition of tri-iodothyronine (T3) production from added thyroxine (T4) in brain, liver and kidney homogenate. This inhibition was reflected in plasma T4 and T3 concentrations, which were respectively increased and decreased in selenium-deficient animals. Although plasma T4 levels increased in selenium-deficient animals, this did not produce the normal feedback inhibition on thyrotropin release from the pituitary. Selenium deficiency was confirmed in the animals by decreased selenium-dependent glutathione peroxidase (Se-GSH-Px) activity in all of these tissues. Administration of selenium, as a single intraperitoneal injection of 200 micrograms of selenium (as Na2SeO3)/kg body weight completely reversed the effects of selenium deficiency on thyroid-hormone metabolism and partly restored the activity of Se-GSH-Px. Selenium administration at 10 micrograms/kg body weight had no significant effect on thyroid-hormone metabolism or on Se-GSH-Px activity in any of the tissues studied. The characteristic changes in plasma thyroid-hormone levels that occurred in selenium deficiency appeared not to be due to non-specific stress factors, since food restriction to 75% of normal intake or vitamin E deficiency produced no significant changes in plasma T4 or T3 concentration. These data are consistent with the view that the Type I and Type II iodothyronine deiodinase enzymes are seleno-enzymes or require selenium-containing cofactors for activity.
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PMID:Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency. 273 May 91

The effects of feeding vitamin E-deficient diets to rats for one year were investigated to analyse the relationship of the vitamin with other antioxidants and some antioxidative enzymes. Long-term vitamin E deficiency lowered the levels of antioxidants like vitamin E, ascorbic acid and glutathione (GSH) in all tissues analysed and thus increasing the extent of tissue peroxidisability. Vitamin E deficiency had also influenced the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase, the enzymes that are involved in detoxification mechanisms of products arising from free radical metabolism.
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PMID:Physiological antioxidants and antioxidative enzymes in vitamin E-deficient rats. 318 81

Lipid peroxidation of rat liver microsomal fractions was monitored by its low-level chemiluminescence in preparations from controls and vitamin-E-deficient animals. Measurements were made (a) of the duration of the lag phase tau0 after initiation with NADPH/iron-ADP and (b) of the slope of the chemiluminescence increase. In microsomes with normal vitamin E (alpha-tocopherol) level the lag phase tau0 was substantially increased by ascorbate; in contrast, even an enhanced peroxidation was observed with ascorbate in vitamin-E-deficient microsomes. Therefore, the ascorbate-mediated protection of microsomal membranes against lipid peroxidation is dependent on vitamin E in the membrane. In vitamin E deficiency the pro-oxidant effect of ascorbate was abolished when glutathione (GSH) was present. Likewise, GSH does not prolong the lag phase tau0 in vitamin E deficiency. However, GSH (but not cysteine) exerts an antioxidant effect both in controls and in vitamin E deficiency by decreasing the slope of the chemiluminescence increase during lipid peroxidation. The involvement of GSH in an enzyme-dependent mechanism is suggested.
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PMID:The protection by ascorbate and glutathione against microsomal lipid peroxidation is dependent on vitamin E. 338 50


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