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 time required for red blood cells (RBC) from vitamin E-deficient lead-poisoned (-E + Pb) rats to pass through polycarbonate filters after incubation in vitro was much greater than that of RBC from vitamin E-supplemented non-poisoned rats. Vitamin E deficiency per se (i.e., in non-poisoned rats) often increased filtration times, but in all such experiments the RBC from -E + Pb groups had even longer filtration times. Administration of lead to rats supplemented with vitamin E had little effect on the filtration rate of RBC. N,N'-diphenyl-p-phenylenediamine (DPPD) prevented the increased filtration times characteristic of RBC from -E + Pb rats, but replacement of the lard in the vitamin E-deficient basal diet by more highly polyunsaturated fats did not exacerbate the increased filtration times of RBC from -E + Pb rats. The increased filtration time of RBC from -E + Pb rats appeared to be related to the extent of RBC lipid peroxidation. Decreasing the pH of the RBC incubation medium from 7.4 to 6.6, an acidity typical of the spleen, markedly increased the filtration times of RBC from -E + Pb rats. Addition of lead in vitro increased filtration times of RBC from both vitamin E-deficient and supplemented non-poisoned rats, but filtration times tended to be longer in the deficient group. These results suggest that vitamin E deficiency and lead toxicity act synergistically to alter the deformability of the RBC thereby rendering it vulnerable to sequestration in the spleen.
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PMID:Filterability of erythrocytes from vitamin E-deficient lead-poisoned rats. 1 50

The dynamics of vitamin E in the blood serum of sows of the Slovak Large White breed was studied from the 10th day of gravidity to the 20th day of lactation. A slight variation was observed in the average values of serum vitamin E from the 10th to the 50th day of gravidity (from 0.134 to 0.122 and 0.129 mg per 100 ml). A rise to the absolutely highest average values of serum concentration of vitamin E, 0.166 mg per 100 ml, was ascertained in the period from the 70th to the 90th day of gravidity. In the subsequent period, i.e. 110th day of gravidity, the value dropped to 0.120 mg per 100 ml, and on the 5th day of lactation the absolutely lowest value (0.095 mg per 100 ml) for the whole study was obtained. On the 20th day of lactation the serum concentration of vitamin E increased on an average to 0.103 mg per 100 ml. These data indicate the critical periods in the levels of vitamin E; these are from the 90th to the 100th day of gravidity and the first days of lactation when the concentration of vitamin E markedly decreases. If vitamin E is not supplemented to the sows during gravidity in sufficient amounts, preclinical and clinical vitamin E deficiency can be expected to occur.
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PMID:[Vitamin E concentration in the blood serum of sows during pregnancy and lactation]. 11 30

The incorporation of 14C-cholesterol into total androgens by testis homogenates and into total androgens and corticosterone by adrenal homogenates was measured in tissues taken from rats deficient in vitamin E, and from rats given vitamin E, from weaning to a maximum of 293 days. The peak of incorporation of 14C into adrenal steroids, androgens and corticosterone, were delayed in the rats deficient in vitamin E, which might suggest a delayed or prolonged period of puberty in vitamin E deficiency. After this period of increased steroidogenesis the deficient rats incorporated consistently less 14C into adrenal steroids and testicular androgens than did the control rats, although the differences were not statistically significant in the experiments described.
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PMID:The effect of vitamin E deficiency on androgen and corticosterone synthesis. 12 72

Rabbits were rendered dystrophic by feeding them a diet deficient in vitamin E and their fast-twitch EDL and slow-twitch SOL muscles were examined histochemically. The soleus muscle of control rabbits consisted largely of type I fibres with occasional areas of scattered type II fibres. In the nutritionally dystrophic rabbits type II fibres were consistently found homogeneously distributed throughout the entire muscle and in increased proportion. A very similar pattern was observed in the solei of rabbits following sciatic nerve section. The normal EDL contained three fibre types (I, IIoxidative and IIglycolytic). Vitamin E deficiency appeared to be associated with a shift towards an increase in the proportion of IIglycolytic fibres at the expense of IIoxidative. In denervation as well as vitamin E deficiency the type I fibres of the EDL appeared to be spared. A small number of the E-deficient rabbits exhibited degenerative changes in their sciatic and sural nerves. When animals were both denervated and E-deprived the resulting muscle changes were very much more severe than in the case of either challenge in isolation. We suggest that although some of the signs of vitamin E deficiency resemble those of a neural defect there is, in addition, a direct myopathic effect.
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PMID:Histochemical changes in fast and slow muscles of nutritionally dystrophic rabbits. 14 84

The objective of this investigation was to find out whether vitamin E deficiency, apart from influencing the lipid component of cellular membranes, also influences the protein component. For that purpose a number of membrane-bound enzymes in the liver of the Pekin duckling were histochemically, cytochemically, and biochemically examined. Furthermore, cells, cellular membranes, and protein particles in membranes were morphometrically investigated. Histochemically five membrane-bound enzymes appeared to be stimulated in vitamin E deficiency: 5'-nucleotidase, glucose-6-phosphatase, isocitrate dehydrogenase (NADP), tetrazolium reductase (NADH), and tetrazolium reductase (NADPH). 5'-Nucleotidase and glucose-6-phosphatase were also investigated cytochemically and biochemically. The cytochemical localization of these enzymes was identical in control and vitamin E-deficient ducklings. Biochemically, a stimulation of these two enzymes also could be demonstrated. The increase per milligram of DNA appeared to be largest whereas the increase per milligram of protein, per milligram of phospholipid, and per milligram of RNA was only half of the increase per milligram of DNA. This can be explained by the 30 per cent increase of the cell volume in vitamin E deficiency leading to an increase of protein, phospholipid, and RNA per cell. The thickness of membranes and the diameter of protein particles in membranes were measured in liver parenchymal cells. In vitamin E deficiency the thickness of the outer mitochondrial membrane and the diameter of protein particles in this membrane were smaller whereas the thickness of the endoplasmic reticular membrane was larger. The increase of the activities of mitochondrial and microsomal enzymes and the decrease of the thickness of the outer mitochondrial membrane and of its protein particles are interpreted to be the result of the influence of free radicals on membranes with electron transport functions. The increase of 5'-nucleotidase activity in the plasma membrane is likely to have a different cause; it may be related to the transport of nucleotides across this membrane.
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PMID:Cellular membranes and membrane-bound enzymes in vitamin E deficiency. A histochemical, cytochemical, biochemical, and morphologic study of the liver of the Pekin duckling. 16 37

The effects of vitamin E deficiency on membrane integrity were studied by examining the temperature dependence of membrane-bound enzyme activities in liver mitochondria and microsome and in muscle sarcoplasmic reticulum. In vitamin E-deficient rabbits, the specific activities at 37 degrees of mitochondrial oligomycin-sensitive ATPase (EC 3.6.1.3), beta-hydroxybutyrate dehydrogenase (EC 1.1.1.30), and microsomal glucose-6-phosphatase (EC 3.1.3.9) were increased, whereas those of microsomal NADH cytochrome C reductase (EC 1.6.99.3) and sarcoplasmic reticulum Ca-ATPase were reduced in comparison to control rabbits. Arrhenius plots of activity against temperature yielded a linear plot over the range 10 to 40 degrees in the case of beta-hydroxybutyrate dehydrogenase, NADH cytochrome C reductase and Ca-ATPase, and multiple discontinuities for glucose-6-phosphatase and oligomycin-sensitive ATPase. In control rabbits, all five enzymes showed a single discontinuity in the Arrhenius plot over the range 16 to 19 degrees. These results reflect changes in the microenvironment of membrane-bound enzymes as a consequence of vitamin E depletion.
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PMID:Effects of vitamin E deficiency on the activities of lipid-requiring enzymes in rabbit liver and muscle. 22 Mar 97

1. The effects of vitamin E deficiency, and of vitamin E and selenium deficiency, on rat liver microsomal aminopyrine demethylase activity were investigated. It was found that, over a wide range of substrate concentrations, the enzyme activity in preparations from deficient animals was significantly lower than that in controls. 2. Addition of antioxidants in vitro, either to the homogenization or to the assay media, was without significant effect on the depressed enzyme activity. Castration and alteration in dietary protein concentration were also without effect. The rate of oxidation of NADPH was however, lower in preparations from deficient animals. 3. Lineweaver-Burk plots of the reciprocal of enzyme activity and substrate concentration showed a higher Km value in preparations from vitamin E-deficient animals, irrespective of whether selenium was present; the Vmax. was unaffected. These parameters were unchanged when antioxidants were added in vitro. Induction with phenobarbitone and 3-methylcholanthrene showed large changes in Km value which, for preparations from vitamin E-deficient animals, was higher than that for corresponding controls. 4. Examination of the synergism between NADH and NADPH as donors of reducing equivalents for aminopyrine demethylation showed that vitamin E and selenium were only minimally involved in the phenomenon. However, both the initial rate and the extent of demethylation were significantly lower in vitamin E- and selenium-deficient preparations and both nutrients were required for the restoration of full activity. 5. The significance of these results is discussed in the light of our working hypothesis.
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PMID:The dependence on vitamin E and selenium of drug demethylation in rat liver microsomal fractions. 23 93

A study was designed to determine if the presence of vitamin E deficiency during the first week of life played a contributory role in the shortened red cell life span observed in the premature infant. Carboxyhemoglobin values were used as an index of hemolysis. Ten infants received vitamin E administered intramuscularly in a total dose of 125 mg/kg during days 3 to 7 of life; ten infants served as controls. The mean percent carboxyhemoglobin level fell significantly from day 3 to day 8 in the treated group (1.08% to 0.78%) whereas the mean value remained unchanged at 0.96% in the control group. The administration of vitamin E appears to reduce but not eliminate the accelerated red cell destruction that characterizes the preterm infant. Pediatrics, 59:995-997, 1677, VITAMIN E, HEMOLYSIS, PREMATURE INFANT, CARBOXYHEMOGLOBIN.
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PMID:Vitamin E and neonatal hemolysis. 32 92

Vitamin E supplementation (dl-alpha-tocopheryl acetate except where noted) in excess of requirement significantly increased humoral immune response or disease resistance. Mice immunized with sheep red blood cells or tetanus toxoid and fed the supplemental vitamin demonstrated increased plaque-forming cells (PFC) and hemagglutinin (HA) titers. A vitamin E deficiency resulted in decreased PFC and little IgG which was partially corrected by N,N-diphenyl-p-phenylenediamine but not as effectively as by vitamin E. Hens immunized with Brucella abortus and fed different levels of the vitamin produced chicks with increased passive immunity; a biphasic antibody response to the level of the vitamin fed was noted. Vitamin E fed to nonimmunized hens was found to significantly increase the primary immune response of their immunized chicks. Feeding dl-alpha-tocopheryl acetate to guinea pigs immunized with Venezuelan equine encephalomyelitis virus resulted in no increased immunity. Injecting this form of the vitamin resulted in severe tissue reaction. However, injecting dl-alpha-tocopheryl significantly improved hemagglutinin inhibition titers. Chicks and turkeys infected with Escherichia coli and fed supplemental vitamin E had reduced mortality and increased HA titers. Sheep fed vitamin E and challenged with Chlamydia had improved weight gains and no detectable Chlamydia.
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PMID:Protective effects of supplemental vitamin E against infection. 37 53

In both animals and humans, vitamin E deficiency is associated with platelet hyperaggregability. In six E-deficient children, thrombocytosis was associated with marked hyperaggregability of their platelets to ADP, epinephrine, and collagen. Platelet malonyldialdehyde (MDA) formation was used as an indicator of prostaglandin formation, and was found to be increased during the E deficiency state. Following E repletion, both platelet aggregation and platelet MDA formation returned to normal. The addition of vitamin E to platelets in vitro has been associated with inhibition of platelet release, aggregation, and MDA formation. Extending these in vitro observations further, six normal controls were given 1600 units of vitamin E orally daily for 2 weeks to elevate their plasma E levels and the E content of their platelets in vivo. Concomitant with the elevation in their plasma E levels, there was an inhibitory effect of 12--20% on platelet MDA formation following E ingestion. These studies suggest that E deficiency increases the in vivo synthesis of platelet endoperoxides and prostaglandins, and that E excess has the opposite effect, i.e., inhibition of the endoperoxide intermediates of prostaglandin synthesis.
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PMID:Vitamin E and platelet function. 39 95


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