Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Deficiencies or disturbances of nutrition cause a variety of diseases and can arise in different ways. The amount of a particular nutrient in the diet may be insufficient to meet the requirements, the diet may contain substances that inactivate the nutrient or inhibit its absorption/utilisation, or metabolism may be upset by the interaction of dietary and environmental factors. Peroxidation of lipids or oxygen free radical generation in general is a physiological process important for cell metabolism, division and differentiation and also for the biosynthesis of hormones and prostaglandins. Free radicals generated through these processes are effectively scavenged by the antioxidant defence system. Uncontrolled lipid oxidation caused by disturbances of that system may play a crucial role in some important poultry diseases and toxicoses. The first route of lipid peroxide loading of the organism is via the feed, such as through oxidised lipids. Oxidised fatty acids are absorbed from the intestine mainly in the form of unsaturated keto compounds and initiate lipid peroxidation in the tissues. The second problem is the insufficient amount of antioxidants in the feed, e.g. vitamin E deficiency. Nutritional encephalomalacia is a problem in poultry production which depends both on the actual vitamin E supply and the dietary amount of polyunsaturated fatty acids. In young birds the primary target of vitamin E deficiency is the brain because it contains low amounts of vitamin E, and the vitamin E content of the liver acting as store decreases rapidly during the first week of life. Besides vitamin E, other components of the antioxidant system, e.g. the antioxidant enzymes (catalase and glutathione peroxidase) also have low activity in the brain as compared to other major tissues. The brain is highly susceptible to oxidative stress because of the accumulation of polyunsaturated fatty acids. The third source of free radical generation is the toxic level of different feed ingredients, e.g. toxicoses caused by vitamin A, selenium, and ionophore antibiotics. Other important aspects of antioxidants (e.g. vitamin E and selenium) in poultry are stimulation of the immune response (e.g. in the case of vaccination) and reduction of the risks of free radical formation as a result of macrophage function.
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PMID:Nutritional metabolic diseases of poultry and disorders of the biological antioxidant defence system. 927 94

Exudative diathesis, a condition caused by a selenium (Se)/vitamin E deficiency, was studied in chicks. Trios of chicks that showed clinical signs of exudative diathesis were matched for severity. One was injected subcutaneously with 0.5 mL distilled water, and the other two received 15 microg of Se in 0.5 mL distilled water. A chick fed a diet with supplemental Se also received 0.5 mL distilled water. Blood was collected from three chicks 2 d after injection, and from the other chick, 6 d after injection. After blood was collected, pectoral muscle and bone marrow were collected. Deficient chicks showed varying degrees of necrosis in pectoral muscle, whereas recovering chicks had extensive fibrosis in pectoral muscle. An analysis of blood showed differences in CO2, glucose, Se, glutathione peroxidase, alanine aminotransferase, aspartate aminotransferase, and creatine kinase. Heterophils and monocytes were increased in deficient chicks; lymphocytes, basophils, and hemoglobin decreased. After 6 d of recovery, all of the changes noted above were correcting toward normal. Eosinophils, in contrast, were unaffected by a deficiency, but increased in recovering chicks. It is hypothesized that cytokines associated with the inflammatory response accentuate the clinical signs of exudative diathesis.
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PMID:Changes in blood chemistry, hematology, and histology caused by a selenium/vitamin E deficiency and recovery in chicks. 963 Apr 19

We investigated the effects of dietary copper and vitamin E in diets containing 6% rapeseed oil on the performance and the antioxidative and oxidative status of growing pigs. The 10 dietary treatments consisted of a basal diet (9 mg of vitamin E/kg feed, 15 mg of Cu/kg feed), the basal diet + 6% rapeseed oil (Diet 1; 18 mg of vitamin E/kg feed, 15 mg of Cu/kg feed), and Diet 1 plus supplements of vitamin E (0, 100, and 200 mg of dl-alpha-tocopheryl acetate/kg feed) and copper (0, 35, and 175 mg of Cu/ kg feed) in a 3 x 3 factorial arrangement of treatments. Eight or nine pigs were given ad libitum access to each diet from 25 to 100 kg of live weight. The inclusion of rapeseed oil tended (P < .10) to improve ADG and feed utilization. Compared with the addition of 35 mg of Cu/kg, the addition of 175 mg/kg improved growth rate and increased feed intake early in the experiment, but, over the total experiment, neither 35 nor 175 mg of Cu/kg affected performance. Compared with the addition of 100 mg of vitamin E/kg or no addition, the addition of 200 mg/kg reduced ADG over the total experiment (P = .05). The antioxidative and oxidative status of the pigs was evaluated in terms of blood and liver concentrations of antioxidants (alpha-tocopherol, ascorbic acid, vitamin A, superoxide dismutase, glutathione peroxidase), prooxidants (Cu), concentrations of lipids (triglycerides and cholesterol), fatty acid composition, thiobarbituric acid-reactive substances (TBARS), and clinical chemical (creatine kinase and glutamate-oxaloacetate-transaminase) and hematological variables that indicate the level of oxidative stress. There were no vitamin E deficiency signs or increased oxidative stress in pigs fed low dietary vitamin E levels, and no prooxidative effect of Cu was found. Increasing dietary levels of vitamin E increased the concentration of alpha-tocopherol in plasma and liver. Supplementation with Cu increased liver concentrations of Cu and alphatocopherol. The progression in liver TBARS was reduced by the addition of vitamin E and Cu. The addition of rapeseed oil changed the fatty acid composition of liver, increased alpha-tocopherol concentration in plasma and Cu concentration in liver, and reduced the rate of lipid oxidation in liver. In conclusion, even though the effects were minor, vitamin E, Cu, and rapeseed oil improved the antioxidative status of the live pigs.
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PMID:Influence of dietary rapeseed oil, vitamin E, and copper on the performance and the antioxidative and oxidative status of pigs. 1032 56

The effect of vitamin E deficiency on glutathione peroxidase activity (GPX) and on the activity of a selenoenzyme (phospholipid hydroperoxide glutathione peroxidase (PHGPX) was measured in rat brain and liver. In brain, the activity of both enzymes was in the same range in homogenate and in microsomes. In contrast, in liver homogenate, PHGPX activity was approximately 20 times lower than that of GPX. Very interestingly, PHGPX activity was significantly decreased in brain microsomes by vitamin E deficiency, but slightly significantly increased in liver microsomes. In contrast, GPX activity was not affected in brain by vitamin E deficiency, but was significantly lower in liver homogenate and microsomes. Thus, PHGPX activity is partially controlled by vitamin E in membranes, and PHGPX is probably an enzyme different from GPX.
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PMID:Vitamin E deficiency has different effects on brain and liver phospholipid hydroperoxide glutathione peroxidase activities in the rat. 1082 43

Selenium and vitamin E deficiencies were studied as part of an evaluation of oxidant defenses in guinea pigs. Male guinea pigs (100-120 g) were fed a control diet (C) or the diet without selenium (0 Se), without vitamin E (0 E), or without either selenium or vitamin E (0 Se-0 E). Between d 30 and 35, 7 of 13 guinea pigs fed the 0 Se-0 E diet were euthanized because of severe weakness of their extremities. No guinea pigs in the other diet groups developed weakness. Guinea pigs from each group were killed on d 37. Selenium deficiency and vitamin E deficiency were verified by measurement of glutathione peroxidase and alpha-tocopherol. Creatine phophokinase (CPK) activity was greater than controls in both groups fed vitamin E-deficient diets, but the increase was greater in the 0 Se-0 E group than in the 0 E group. Muscle F(2)-isoprostanes were greater than controls in both groups fed vitamin E-deficient diets with the level in the 0 Se-0 E group greater than that in the 0 E group. Histologic muscle necrosis was severe in the 0 Se-0 E group, minimal in the 0 E group and absent from other groups. The diets used in this study induced selenium and vitamin E deficiencies in guinea pigs. The study demonstrates that combined selenium and vitamin E deficiency results in a fatal myopathy in guinea pigs that is associated with lipid peroxidation in the affected muscle. This nutritional myopathy is much more severe than the myopathy that occurs with vitamin E deficiency alone.
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PMID:Combined selenium and vitamin E deficiency causes fatal myopathy in guinea pigs. 1138 70

Necrosis and apoptosis coexist in the thyroid during goitre development and involution, but little is known about their respective causes. To test the possible role of free radicals, we analysed separately necrosis and apoptosis in male Wistar rats with depressed or normal antioxidant protection. Vitamin E-deficient and -sufficient rats were made goitrous with perchlorate in drinking water; involution was induced by repeated injection of NaI, without or with methimazole. Increase of thyroid malondialdehyde concentration and decrease of glutathione peroxidase activity confirmed the depressed antioxidant protection in vitamin E-deficient rats. Plasma thyroxine and TSH levels were not modified. Necrosis (swollen cells) and apoptosis (pyknotic cells) were quantified on histological sections. In vitamin E-sufficient rats, dead cells were very rare in control thyroids, increased 3-fold in goitre and still further during involution. Necrotic epithelial cells predominated in the goitre and their number declined after iodide supplementation, without or with methimazole. In contrast, the number of apoptotic cells and the caspase-3 activity were increased in goitre and further increased after involution, with two-thirds of pyknotic cells being observed in the interstitium. Apoptosis was prevented by methimazole. Vitamin E deficiency significantly increased total cell death and epithelial cell necrosis and induced the occurrence of much cell debris in the follicular lumen during involution, with no modification of the apoptotic reaction. These results show that the type of cell death is differentially regulated during goitre development and involution: necrosis is related to the oxidative status of the cells, while apoptosis comes with iodine-induced involution.
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PMID:Cell necrosis and apoptosis are differentially regulated during goitre development and iodine-induced involution. 1183 55


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