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

Effects of a short-term vitamin E deficiency on some lipid peroxidative properties were investigated in mouse cardiac and skeletal muscles. The concentration of vitamin E decreased 35.8% in 5 weeks and 61.2% in 12 weeks in skeletal muscle. The corresponding decrease in cardiac muscle was 65.7% in 12 weeks. Simultaneously the susceptibility of muscle homogenates to in vitro lipid peroxidation increased with 48.6% (5 weeks) and 44.5% (12 weeks) in skeletal muscle and with 101.8% (12 weeks) in cardiac muscle. Highly significant negative correlations were observed between the concentration of vitamin E and in vitro lipid peroxidation in cardiac and skeletal muscles. Also the sensitivity to Fe2+-induced peroxidation was increased in skeletal muscle after the deficiency of 5 weeks. The total contents of peroxidizable lipids (Fe2+-induction) were significantly (approx. 20%) decreased after 12 weeks in cardiac and skeletal muscles. The concentration of lipofuscin was unaffected in both muscles of vitamin E-deficient mice. Vitamin E deficiency (5 weeks) decreased the activity of selenium-dependent glutathione peroxidase in skeletal muscle but did not affect the activities of catalase and beta-glucuronidase and the concentrations of protein, reduced glutathione and total sulfhydryl groups. These results show that a short-term vitamin E deficiency affects the peroxidative properties of cardiac and skeletal muscles and may thus expose the muscles to peroxidation injuries.
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PMID:Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles. 652 97

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

The effects of parenteral vitamin E treatment on aspects of the pulmonary biochemical and morphologic response to 100% oxygen were studied in newborn rabbits manifesting chemical evidence of vitamin E deficiency. Pups treated with 2 mg/100 g body weight increased serum vitamin E levels from 0.39 to 2.17 mg/dl by 72 hr and lung tissue vitamin E content from 3.52 to 17 mg/mg wet weight of lung. In vitro lipid peroxidation in lung homoginates of animals in 100% oxygen for 72 hr was inhibited by approximately 80% in animals receiving 100% oxygen plus vitamin E. Hyperoxia-induced increases in the pulmonary antioxidant enzymes, superoxide dismutase, glutathione peroxidase, and glutathione reductase were diminished by vitamin E administration. Lungs from vitamin E-treated animals did not show the early lung epithelial injury seen in animals exposed to 100% oxygen but not treated with vitamin E. Mophometric analysis of lungs of animals in room air for 72 hr showed 81.6% of lung to be normal as compared with 43.3% normal lung in the group maintained in 100% oxygen for 72 hr. In the group treated with oxygen plus vitamin E, the lungs were similar to room air controls (82.6% normal). This study thus provides further evidence for a direct antioxident affect of vitamin E in lung.
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PMID:Vitamin E affects lung biochemical and morphologic response to hyperoxia in the newborn rabbit. 722 Jan 49

1. Glutatione peroxidase activity (EC 1.11.1.9) and erythrocyte stability were measured in Friesian bull calves which were given for 36 weeks semi-purified diets either adequate or low in selenium or vitamin E or both. 2. Dietary Se or vitamin E content had no effect on growth rate and haematlogical values. None of the calves exhibited clinical deficiency symptoms and serum aspartate amino transferase (EC 2.6.1.1) and creatine phosphokinase (EC 2.7.3.2) activities remained normal. Heart and skeletal muscles of all calves appeared macroscopically and microscopically normal ato autopsy. 3. Glutathione peroxidase activity in plasma, blood and other tissues, except the testis, was significantly lower in calves receiving low dietary Se but was independent of dietary vitamin E content. 4. Plasma vitamin E levels decreased rapidly and to very low levels in calves given low vitamin E diets irrespective of the Se content of the diet. 5. A low dietary vitamin E intake increased the susceptibility of erythrocytes to auto- and peroxidative haemolysis whereas a low Se intake in the presence of adequate vitamin E did not. However, erythrocytes from calves receiving low Se and low vitamin E were more susceptible to peroxidative haemolysis than erythrocytes from calves receiving low vitamin E and adequate Se. The effect of dietary vitamin E content on osmotic haemolysis induced by hypotonic saline was variable. 6. The results suggest that measurement of blood glutathione peroxidase activity and the susceptibility of erythrocytes to auto- or peroxidative haemolysis could be used for the differential diagnosis of subclinical Se and vitamin E deficiency in ruminants.
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PMID:Glutathione peroxidase activity and erythrocyte stability in calves differing in selenium and vitamin E status. 728

A survey of selenium and vitamin E concentrations in horses was conducted at four breeding farms in New York. There were no significant changes in mean blood selenium concentrations in horses at the three sampling dates whereas vitamin E concentrations underwent seasonal fluctuations. The mean blood selenium concentration in this survey for horses fed local feed was 7.7 microgram/dl. Horses fed commercial feed had a mean blood selenium concentration of 15.6 microgram/dl. A 0.94 correlation coefficient was found between blood glutatione peroxidase activity and blood selenium concentrations in horses. The effect of oral and parenteral selenium administration on blood selenium concentrations and blood glutathione peroxidase activity was also investigated. Oral supplementation of 1 mg selenium per day increased blood selenium concentrations above levels associated with myodegeneration in horses and foals. Parenteral supplementation trials with mares at late gestation indicate that only limited amounts of selenium cross the placental barrier. Parenteral supplementation of mares during gestation and lactation or supplementation of foals beginning at birth will increase blood selenium levels in foals above that associated with selenium/vitamin E deficiency.
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PMID:Selenium and vitamin E in horses. 742 74

The effects of oxygen inhalation for 48 h on the antioxidant capacity of lungs, livers, and brains in normal and vitamin E-deficient rats at various ages were examined. The activity levels of catalase, glutathione peroxidase, and superoxide dismutase, and the level of vitamin E in tissue homogenates were assayed as the indices of antioxidant capacity. Oxygen inhalation mostly decreased antioxidant enzyme activity in lungs. In particular, the catalase activity was much decreased. The glutathione peroxidase activity tended to be decreased. The superoxide dismutase activity was decreased in 32-month-old rats. Vitamin E deficiency did not augment oxidative damage due to oxygen inhalation. There appears to be no age effect on the oxygen-induced decrease in the antioxidant enzyme activities of lungs, except the superoxide dismutase activity in very old rats. Oxygen inhalation had some effects on the antioxidant capacity of livers and brains. For example, oxygen inhalation decreased the vitamin E concentration of livers in 32-month-old, normal rats. These results suggest that the antioxidant capacity of lungs is directly damaged by oxygen inhalation and that the antioxidant capacity of livers and brains is indirectly affected through lung damage. Antioxidant capacity may be maintained without large variation during young and middle ages, but its redundancy for emergency use may be diminished in old age.
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PMID:Effects of oxygen inhalation on the antioxidant capacity of lungs, livers, and brains in normal and vitamin E-deficient rats at various ages. 761 20

The activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) and free radicals were measured, and the morphological changes were observed in the lens of control rats, selenium-deficient (SeD) and/or vitamin E deficient (VED) rats. The activities of GSH-Px in the lens of SeD rats decreased significantly. The GSH-Px activities of lens were positively related to erythrocytes selenium level. There was a free radical at g = 2.0015 in the rat lens of all groups, but the content of free radicals in the lens of SeD group was significantly higher than that of the control group. The free radical content of lens was negatively related to erythrocytes selenium level, as well as the GSH-Px activities in the lens. In vitro, ultraviolet radiation caused the generation of another kind of free radical (g = 2.0097) in the lens of all groups, but the amount of the free radical in the lens of the SeD group was also significantly higher than that of the control group. The activities of SOD and GSSG-R in VED rat lens were significantly decreased. The amount of MDA in the lens of SeD and/or VED rats were significantly increased. The results showed that the decrease of antioxidative capability in the lenses of SeD and/or VED rats accelerated the lipid peroxidation and generation of free radicals. Although only early morphological changes in SeD and/or VED rat lens were observed, it is considered that selenium and vitamin E deficiency may be involved in the occurrence of cataract.
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PMID:Biochemical and morphological changes in the lenses of selenium and/or vitamin E deficient rats. 794 5

The aim of the present study was to investigate whether the level of selenium and selenium/vitamin E supply influences the humoral immunity of rats. In order to detect the effect of Se supply and age, 36 weaned Sprague-Dawley rats divided into two equal groups were killed after 22 or 45 experimental days by decapitation (Exp. I). In Exp. II 9 groups of 10 rats each were exposed to each combination of deficient, normal or excessive selenium with a vitamin E supply and killed after 44 days. The basic (deficiency) diet which was the same in both experiments contained 0.04mg Se and 8mg vitamin E per kg dry matter. The supplementation per kg diet was 0 or 0.2mg Se and 30mg vitamin E in Exp. I and 0, 0.2 or 1mg Se and 0, 30 or 200mg vitamin E in Exp. II. The concentration of selenium in serum, liver and spleen samples and the activity of glutathione peroxidase, which were determined to define the selenium status of the animals, corresponded well to the required supply situation. The immunoglobulins of type IgA, IgM and IgG with the subtypes IgG1, IgG2a, IgG2b and IgG2c were measured by immunoelectrophoresis. In both experiments selenium deficiency decreased the values of the IgG groups only nominally, IgA was not changed. IgM was significantly reduced, especially with prolonged selenium deficiency and simultaneous vitamin E deficiency. An excessive selenium supply compensated to a great extent for the effects of vitamin E deficiency on IgG and IgA.
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PMID:Effects of different levels of dietary selenium and vitamin E on the humoral immunity of rats. 815 86

Over a period of 4 wk, 24 10-d-old broiler hens were fed diets containing 11% vegetable oil (9% rapeseed oil, 2% soybean oil), which was added either fresh (1 meq O2/kg oil) or oxidized (156 meq O2/kg oil). The effects of the dietary treatments on nutrient digestibility were examined in a balance experiment. The antioxidative status of the animals was evaluated using plasma concentrations of thiobarbituric acid-reactive substances (TBARS), erythrocyte hemolysis in vitro, selenium-dependent and selenium-independent activity of glutathione peroxidase in liver cell cytosolic fractions, and concentrations of tocopherols and other fat-soluble compounds with antioxidative properties (lutein, beta-carotene, and retinol) in plasma and various tissues (skeletal muscle, cardiac muscle, liver, and abdominal fat). Compared to the fresh oil, the concentrations of linoleic and linolenic acid were slightly lower in oxidized oil. The concentration of alpha-tocopherol in the diet with fresh oil was an average of 80.8 mg/kg diet, whereas the diet with oxidized oil only provided 44 mg/kg. The dietary selenium content averaged 0.48 mg/kg in both diets. During the experiment, none of the animals showed symptoms of diarrhea or vitamin E deficiency. The intake of oxidized oil caused a growth depression after 2 wk. The retention of fat (P = 0.07), energy (P = 0.09), and alpha-tocopherol (P < 0.01) was lower in the group fed oxidized fat. Furthermore, these animals showed significantly higher plasma concentrations of TBARS (P < 0.01), and lower concentrations of tocopherols, lutein, beta-carotene, and retinol in plasma and tissues.
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PMID:Inclusion of oxidized vegetable oil in broiler diets. Its influence on nutrient balance and on the antioxidative status of broilers. 882 33

The hepatic and pulmonary effects of nitrofurantoin (40 mg/kg, intraperitoneally) were determined at 4 and 24 hr following its administration in mice fed for 10 weeks with a vitamin E sufficient, deficient or enriched diet. Liver glutathione (GSH) was reduced by nitrofurantoin at 4 hr but was unchanged 20 hr later. Nitrofurantoin did not affect liver glutathione peroxidase, glutathione reductase or superoxide dismutase activities. Liver catalase activities were decreased by nitrofurantoin at 4 hr. Lung GSH levels were increased whilst glutathione peroxidase activity was decreased at 4 and 24 hr. Lung glutathione reductase activity was reduced in certain groups. Nitrofurantoin did not affect lung superoxide dismutase, but catalase was decreased at 24 hr. Liver malondialdehyde levels were increased by nitrofurantoin in the vitamin E deficient group whilst lung malondialdehyde levels remained unchanged. Both liver and lung malondialdehyde levels were unaffected by vitamin E supplementation when compared to the vitamin E-sufficient group. These results suggest that nitrofurantoin (40 mg/kg) was deleterious to the liver and lung. Nitrofurantoin-induced lipid peroxidation was seen in vitamin E deficiency but an increase in dietary vitamin E content did not provide additional protection compared to the recommended daily allowance. The antioxidant activities of alpha-tocopherol and gamma-enriched tocotrienol were similar.
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PMID:Nitrofurantoin-induced hepatic and pulmonary biochemical changes in mice fed different vitamin E doses. 900 Feb 62


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