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

The effects of 10 weeks of dietary selenium and/or vitamin E deficiency (< 0.03 mg Se and 1.5 mg vitamin E per kg diet) on body Se and vitamin E stores and on the down-regulation of liver cellular glutathione peroxidase (GPx1) and plasma glutathione peroxidase (GPx3) were examined in growing female New Zealand White rabbits in comparison to Se (+ 0.40 mg Se/kg diet) and/or vitamin E (+ 150 I.U./kg diet) supplemented controls. Additionally plasma lactate dehydrogenase (LDH) activity, liver thiobarbituric acid-reactive substances (TBA-RS) and liver protein carbonyls were measured to assess the development of oxidative stress during an alimentary Se and/or vitamin E deficiency. Significantly decreased concentrations of Se and vitamin E in plasma (Se: - 70%; vitamin E: - 87%) and liver (Se: - 90%; vitamin E: - 95%) indicated an efficacious Se and vitamin E depletion of the rabbits within 10 weeks. GPx1 messenger RNA levels (GPx1 mRNA) in the livers of Se-depleted rabbits were down-regulated to 1/3-1/8 of the Se supplemented controls. GPx1 enzyme activity in the livers of Se-deficient rabbits declined to 10% of the Se-supplied control rabbits. A significantly elevated LDH activity in the blood plasma of Se- and vitamin E-deficient rabbits indicated a general impairment of tissues. Markedly increased TBA-RS concentrations and protein carbonyl contents in the livers of Se- and vitamin E-deficient rabbits gave further evidence for severe oxidative damage of cellular lipids and proteins during an alimentary Se and/or vitamin E deficiency. Both a full expresssion of GPx1 attained by dietary Se supplementation and dietary vitamin E supply effected an almost complete protection against oxidative cellular damage of the liver.
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PMID:Down-regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium-deficient rabbits. 1245 69

Five young adult pet marmosets (Callithrix spp.) were presented with weight loss (5/5); fecal retention (3/5); diarrhea (2/5); impaired locomotion (3/5); anemia (4/4); hypoproteinemia or hypoalbuminemia (3/4); elevations of creatine phosphokinase, lactic dehydrogenase, and alanine aminotransferase (3/4); and renal failure with hypercholesterolemia (2/4). All anemic marmosets had low serum vitamin E levels. The anemia responded to vitamin E and selenium therapy in two marmosets. One of the five marmosets died before presentation, and two others died despite therapy. The two marmosets necropsied had degenerative myopathy, pyogranulomatous pansteatitis, and increased erythrophagocytosis and hemosiderosis. The striated muscle and adipose tissue of both marmosets were negative for coxsackievirus ribonucleic acid by in situ hybridization. These findings suggest that vitamin E deficiency may be involved in the development of anemia, myopathy, and steatitis in callitrichids; however, in some marmosets, underlying diseases such as chronic colitis may have influenced the development of anemia and impaired vitamin E status.
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PMID:Anemia, myopathy, and pansteatitis in vitamin E-deficient captive marmosets (Callithrix spp.). 1294 11

Mitochondria clearly play a central role in the pathogenesis of Friedreich's Ataxia. The most common genetic abnormality results in the deficiency of the protein frataxin, which is targeted to the mitochondrion. Research since this discovery has indicated that mitochondrial respiratory chain dysfunction, mitochondrial iron accumulation and oxidative damage are important components of the disease mechanism. While the role of frataxin is not known, evidence is currently pointing to a role in either mitochondrial iron handling or iron sulphur centre synthesis. These advances in our understanding of the disease mechanisms are enabling therapeutic avenues to be explored, in particular the use of established drugs such as antioxidants and enhancers of respiratory chain function. Vitamin E therapy has been shown to be beneficial in patients with ataxia with vitamin E deficiency, and CoQ10 therapy was effective in some patients with ataxia associated with CoQ10 deficiency. A combined therapy involving long term treatment with high doses of vitamin E and coenzyme Q10 has jointly targeted two of the major features of Friedreich's Ataxia; decreased mitochondrial respiratory chain function and increased oxidative stress. This therapy clearly showed a rapid and sustained increase in the energy generated by the FRDA heart muscle, nearly returning to normal levels. The improvements in skeletal muscle energy generation parallel those of the heart but to a lower level. While this therapy appeared to slow the predicted progression of some clinical symptoms a larger placebo controlled study is required to confirm these observations. Other antioxidant strategies have involved the use of Idebenone, selenium and N acetyl cysteine but only the use of Idebenone has involved structured trials with relatively large patient numbers. Idebenone clearly had an impact upon the cardiac hypertrophy in the majority of patients, although there have not been any other significant benefits reported to date.
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PMID:Friedreich's Ataxia: disease mechanisms, antioxidant and Coenzyme Q10 therapy. 1469 32

A sheep flock experienced losses in weaned lambs from myopathy and hepatic lipidosis. Investigation revealed painful ambulation, illthrift, and unexpected death in lambs with normal selenium levels, deficient vitamin E levels, and elevated muscle and liver enzyme levels. Vitamin E deficiency should be considered when investigating myopathy and illthrift in lambs.
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PMID:Myopathy and hepatic lipidosis in weaned lambs due to vitamin E deficiency. 1507 98

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

A study was undertaken to indicate the importance of different causes of death in goats and to investigate the management factors which influence these problems. Over a 15 month period, 324 dead goats were received from 67 farms in the Horowhenua, Wairarapa, Wanganui and Wellington regions. Although a wide range of diseases was encountered in the study, the major causes of mortality could be divided into 4 groups: problems directly related to management, microbial diseases, nematode parasitism, and trace element related deficiencies and toxicities. The highest proportion of deaths related directly to management problems and included deaths from hypothermia, mismothering, premature birth, ruminal acidosis, pregnancy toxaemia, trauma, and plant and chemical toxicities. In larger flocks, microbial diseases including Pasteurella pneumonia and yersiniosis were major problems. Deaths from nematode parasitism were predominantly observed in goats 12 months of age and older. White muscle disease (selenium/vitamin E deficiency) was the major trace element deficiency causing death in goats. The influence of factors including age of goat, flock size and management practices on the major causes of death are discussed.
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PMID:A goat mortality study in the southern North Island. 1603 83

The objective of this study was to investigate the effects of selenium (Se) and alpha-tocopherol supplementation on uterine involution and ovarian function in dairy heifers fed a prepartum diet containing low concentrations of Se and alpha-tocopherol. Twenty-four pregnant Friesian heifers were randomly allocated to one of four experimental groups in a 2 x 2 design balanced for age and body weight. Prepartum treatments consisted of supplementation with either 2 intraruminal Se pellets or 3600 mg of alpha-tocopherol p.o. 4 times per wk, or both. Control animals received no supplementation. For 8 wk before calving, the heifers were fed exclusively on pasture hay which contained less than 10 microg/kg of Se and 19 mg/kg of alpha-tocopherol. After calving, the heifers grazed perennial ryegrass and white clover pasture. Concentrations of Se and alpha-tocopherol in serum for the prepartum heifers of the control group were 10 ng/ml and 1.3 microg/ml, respectively, indicating deficiencies of these nutrients. Treatment with Se and alpha-tocopherol increased prepartum serum concentrations of Se and alpha-tocopherol to 74 ng/ml and 5 microg/ml, respectively (P < 0.001). However, treatment with Se, alpha-tocopherol, or both, failed to enhance uterine involution, hasten resumption of postpartum ovarian activity or reduce the incidence of clinical postpartum abnormalities. These findings suggest that postpartum reproductive dysfunction is not a primary feature of moderate Se or vitamin E deficiency of cattle at pasture.
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PMID:Effect of selenium and a-tocopherol supplementation on postpartum reproductive function of dairy heifers at pasture. 1672 17

Undernutrition or malnutrition adversely affects host defenses against many invading microorganisms, thereby increasing the severity of infection. Studies of RNA viruses (e.g., coxsackievirus B and influenzavirus) have shown that selenium or vitamin E deficiency in mice increases disease severity and results in stable genomic changes in the virus that increase virulence. Changes in H3N2 influenzavirus were predominantly in the ordinarily stable M1 matrix protein. Whether this represents selection of already-existing variants or direct effects on viral RNA is unclear. Related questions include whether undernutrition in persons who acquire infection with influenzavirus H5N1 could promote genomic changes during infection that result in greater virulence and higher case-fatality rates, and whether undernutrition could help create the multiple mutations needed to instigate human-to-human transmission. These possibilities emphasize the importance of alleviating world poverty and malnutrition. In addition, these findings suggest that the neglected area of undernutrition affecting invading microorganisms merits intensive investigation in humans and experimental models.
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PMID:Undernutrition can affect the invading microorganism. 1763 96

Selenium (Se) and vitamin E are antioxidant micronutrients. Se functions through selenoproteins and vitamin E reacts with oxidizing molecules in membranes. The relationship of these micronutrients with the Nrf2-antioxidant response element (ARE) pathway was investigated using ARE-reporter mice and Nrf2-/- mice. Weanling males were fed Se-deficient (0 Se), vitamin E-deficient (0 E), or control diet for 16 or 22 weeks. The ARE reporter was elevated 450-fold in 0 Se liver but was not elevated in 0 E liver. Antioxidant enzymes induced by Nrf2-ARE (glutathione S-transferase (GST), NAD(P)H quinone oxidoreductase (NQOR), and heme oxygenase-1 (HO-1)) were elevated in 0 Se livers but not in 0 E livers. Deletion of Nrf2 had varying effects on the inductions, with GST induction being abolished by it but induction of NQOR and HO-1 still occurring. Thus, Se deficiency, but not vitamin E deficiency, induces a number of enzymes that protect against oxidative stress and modify xenobiotic metabolism through Nrf2-ARE and other stress-response pathways. We conclude that Se deficiency causes cytosolic oxidative stress but that vitamin E deficiency does not. This suggests that the oxidant defense mechanisms in which these antioxidant nutrients function are independent of one another.
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PMID:Selenium deficiency activates mouse liver Nrf2-ARE but vitamin E deficiency does not. 1827 78


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