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

The metabolic relationships among the antioxidant nutrients selenium, sulfur, and vitamin E are particularly close. Selenium and vitamin E have long been known to spare one another in certain nutritional diseases of animals, and selenium has been considered to have a key antioxidant defense function as a component of glutathione peroxidase. However, the antioxidant role of glutathione peroxidase has been questioned and new proteins containing selenium have been identified: phospholipid hydroperoxide glutathione peroxidase, selenoprotein P, and iodothyronine deiodinase. Glutathione peroxidase activity independent of selenium resides in the glutathione S-transferases. Glutathione participates in both enzymatic and nonenzymatic antioxidant defense systems. Some low-molecular weight selenium compounds (e.g., ebselen) exhibit glutathione peroxidase-like action. Certain low molecular weight thiols decompose peroxides nonenzymatically (e.g., the ovothiols). Murine malaria appears to be a useful experimental model for investigating interrelationships of selenium and vitamin E. Vitamin E deficiency protects against the parasite, especially when the mice are concurrently fed peroxidizable fat such as fish or linseed oils. Selenium deficiency, on the other hand, has little or no protective effect against the parasite. Any practical utility of pro-oxidant diets in combating human malaria remains to be determined.
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PMID:Selenium and sulfur in antioxidant protective systems: relationships with vitamin E and malaria. 157 91

1. Food selenium content, selenium supply and selenium needs are presented, along with methods of evaluation of selenium status. Glutathione peroxidase, a selenium-containing enzyme, is ubiquitous in the organism. 2. Some experimental studies on animal models reported a positive relationship between selenium status and resistance against infections. 3. Only one study in humans concerned the mechanisms of immune functions in selenium deficiency. Several experimental works suggest that severe selenium deficiency compromises T-cell dependent immune functions such as the blastogenic response to mitogens, but selenium deficiency was concomitant with vitamin E deficiency in most of them. Delayed hypersensitivity response is controversial in selenium-supplemented rats and guinea-pigs. 4. Selenium deficiency in animals decreases the antibody response, especially if associated with vitamin E deficiency. Low dietary selenium supplementation of healthy animals has a positive effect upon humoral responses. 5. Despite some controversies, most experimental studies on selenium-deficient animals report normal phagocytosis and an altered bactericidal capacity of neutrophils. The decrease in glutathione peroxidase activity of polymorphonuclear cells following selenium deficiency could explain some of these alterations. 6. Splenic Natural Killer cells activity is enhanced in selenium-supplemented, healthy animals.
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PMID:Relationship between selenium, immunity and resistance against infection. 198 Apr 38

There is increasing evidence that islet beta cells may be susceptible to redox insult, and that this susceptibility may contribute to the pathogenesis of experimental models of diabetes mellitus. We investigated the effect of vitamin E deficiency, selenium deficiency, and combined deficiency on islet function and free radical scavenging systems. The tissue levels of glutathione peroxidase, catalase, and immunoreactive superoxide dismutases were measured in four groups of rats (i.e., controls and those with vitamin E, selenium, and combined deficiency). Glucose tolerance tests were performed for each animal before sacrifice. Superoxide dismutase concentrations in liver, heart, and skeletal muscle were within 20% of the control levels in all groups. However, the manganosuperoxide dismutase concentrations in islets were significantly lower than control levels in response to vitamin E, selenium, and combined deficiency. Combined deficiency appeared to have an additive effect. In contrast, cuprozinc superoxide dismutase concentration in islets was higher in the deficient groups than in controls. Insulin secretory reserve was decreased in each of the three deficient groups. This decrease was reflected as glucose intolerance only in the group with combined deficiency. Glutathione peroxidase activity was markedly decreased in selenium-deficient animals in all tissues studied. Catalase activity did not change significantly among groups in any tissue studied. Islets had the lowest glutathione peroxidase and cuprozinc and total superoxide dismutase levels among tissues studied.
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PMID:Effect of vitamin E deficiency and selenium deficiency on insulin secretory reserve and free radical scavenging systems in islets: decrease of islet manganosuperoxide dismutase. 351 3

Glutathione peroxidase (EC 1.11.1.9.) (GSHPx) and P-450 activity were measured in hepatic mitochondrial and microsomal fractions from rats deficient in vitamin E and/or essential fatty acids (EFA). The data were compared to corresponding normal values. GSHPx was significantly decreased in the mitochondrial matrix from animals in all 3 deficiency states. In vitamin E deficiency, a non-significant decreased GSHPx activity was found in mitochondrial membranes. Opposite to these findings, GSHPx was significantly increased in mitochondrial membranes of EFA-deficient animals. In combined EFA and vitamin E deficiency, the mitochondrial membrane GSHPx activity was only insignificantly increased. The P-450 complex activity was not detectable in the mitochondrial matrix. In mitochondrial membranes and microsomes, the P-450 complex activity changed parallel to the GSHPx activity.
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PMID:Subcellular distribution of the cytochrome P-450 complex and glutathione peroxidase activity in vitamin E and essential fatty acid deficiency. 645 38

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

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