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

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

Beginning at hatching, male Cornell K strain single comb white leghorn chickens were fed a basal diet, with or without vitamin E (100 IU/kg) and/or selenium (Se, 0.2 ppm). After 3 weeks of treatment, animals fed either the Se-deficient or basal diet had significantly reduced plasma Se-dependent glutathione peroxidase activities when compared to those fed a vitamin E and Se-supplemented diet. Similarly, animals fed the vitamin E-deficient or basal diet had significantly reduced plasma alpha-tocopherol levels. The effect of these treatments on plasma concentrations of thyroid hormones (T(3)/T(4)), growth hormone (GH), and thymic hormone (thymulin) was determined using radioimmunoassay and ELISA. A deficiency in Se, but not in vitamin E, resulted in an increase in plasma T(4) concentrations while plasma T(3) concentrations were decreased. Plasma GH levels showed some fluctuation as a result of the dietary treatments but there was no significant correlation between plasma GH levels and any of the other variables. A significant decrease in plasma thymulin levels was observed in Se-deficient birds compared to those receiving adequate Se in the diet. A vitamin E deficiency had no measurable effect on plasma thymulin levels. From these studies, we conclude that plasma thymulin concentrations directly correlate with plasma T(3) concentrations which are negatively affected by a Se deficiency.
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PMID:The effects of dietary vitamin E and selenium deficiencies on plasma thyroid and thymic hormone concentrations in the chicken. 1557 74

Several oxidative stressors (dietary selenium deficiency, dietary vitamin E deficiency coupled with fish oil feeding, genetic reduction of glutathione peroxidase activity) allow a normally benign coxsackievirus B3 (CVB3/0) to damage heart muscle in host mice. This study investigated whether dietary iron overload, another oxidant stress, would also permit CVB3/0 to exert a cardiopathologic effect in vitamin E-deficient (-VE) mice. Four groups of mice were fed either a -VE or a +VE diet containing either an adequate or an excessive (30x) amount of iron. After 4 weeks of feeding, the mice were inoculated with CVB3/0 and heart damage was assessed at various times postinfection. Mice fed a diet sufficient in VE with excess iron developed heart damage equivalent to mice fed a diet deficient in vitamin E without excess iron. However, severe heart damage occurred in the group fed a diet deficient in VE with excess iron, which was the most pro-oxidative diet. The highest heart viral titers were found in mice fed the -VE/excessive iron diet. However, the extent of heart damage did not always correlate with the formation of TBARS in liver homogenates. Further research is needed to clarify the role of oxidative stress and iron overload in determining the course of viral infection.
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PMID:Benign coxsackievirus damages heart muscle in iron-loaded vitamin E-deficient mice. 1558 79

The role of dietary Cu and Mn in maintaining tissue integrity, through the effects of these metals on activity of the superoxide dismutase (SOD) enzyme, and their interactions in peroxidative pathways involving Se and vitamin E was investigated. Weanling rats were fed diets deficient in Mn, Cu, Se, and/or vitamin E for 35 days, in a factorial experimental design. Dietary effects on peroxidation, measured in mitochondrial fractions prepared from liver and heart tissue, were compared with changes in the activities of glutathione peroxidase and the Cu and MnSOD enzymes.Decreased heart MnSOD and CuSOD activities, resulting from dietary Mn and Cu deficiencies, were both associated with increased peroxidation. Adequate Se (and glutathione peroxidase activity) prevented the peroxidation associated with either of these deficiencies, but was ineffective with a combined Cu-Mn deficiency. These effects of Se were only observed in tissue lacking glutathione transferase activity. Effects of Cu, Mn, and Se on peroxidation appeared to be present at both levels of vitamin E, although in both tissues, vitamin E deficiency greatly increased the overall peroxidation. Comparison of these in vitro peroxidation results with the deficiency associated lesions observed in vivo indicates that changes in SOD activities and peroxidation pathways may be the dominant cause of these lesions in only some cases. In others, the roles of Cu and Mn in different metabolic pathways appear to be of greater importance.
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PMID:The role of dietary copper, manganese, selenium, and vitamin E in lipid peroxidation in tissues of the rat. 2427 94

Successful implantation of an embryo requires adequate depth of invasion in the endometrium, which depends upon decidualization. The aim of the present study was to elucidate why humans experience spontaneous decidualization and menstruation while most other mammals do not. We established a spontaneous decidualization model in pseudopregnant rats with vitamin E deficiency (VED) to investigate mechanisms associated with spontaneous decidualization. Vaginal smears were used to monitor bleeding while vitamin E levels were analyzed with a commercial vitamin E assay kit. Trypan blue staining was used to observe the implantation site at 5.5 days post-coitum (dpc). Uterine morphology, estradiol (E2) and progesterone levels, and the anti-oxidation system were evaluated at 5.5, 7.5, and 9.5 dpc. The proportion of rats in the VED group exhibiting endometrial bleeding gradually increased (5.9%, 32.3%, and 50%) over three consecutive cycles of pseudopregnancy. Vitamin E levels in the VED group were markedly lower compared to the control group in both the plasma and uterus, while the level of vitamin E in the liver did not differ between the control and VED groups. Spontaneous decidualization in the VED group was validated by histological examination and immunohistochemistry. At 5.5 dpc, the mean serum E2 level in the VED group was more than twice that of the control group. The mean total anti-oxidizing capability, catalase level, and glutathione peroxidase activity were significantly reduced in the decidualized portion of the VED group compared to controls, while the malondialdehyde level was also significantly higher in the decidualized portion of the VED group. We hypothesize that the E2 surge at 5.5 dpc and increasing levels of reactive oxygen species are responsible for spontaneous decidualization in VED rats.
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PMID:Spontaneous decidualization in pseudopregnant rats with vitamin E deficiency. 2703 6


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