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At least 19 recordsLinked to original sources
PubMed1976

The influence of vitamin E deficiency and combined deficiency in vitamin E and polyunsaturated fatty acids on the biosynthesis and degradation of rat central nervous system myelin.

The ability to incorporate intracranially injected 14C-labelled leucine into central nervous system (CNS) myelin was studied in developing rats fed a control diet, a diet deficient in vitamin E and a diet deficient both in vitamin E and polyunsaturated fatty acids. The turnover of radioactivity incorporated into myelin and the distribution of radioactivity between the individual proteins of rat CNS myelin at various stages of the deficiency state was studied. Impaired myelin formation was found in cases of both types of deficiency. The level of incorporated radioactivity was raised by both types of deficiency throughout the experimental period. The mean half life of myelin radioactivity was found higher in combined deficient animals as compared to control and vitamin-E-deficient rats. The distribution of radioactivity between myelinproteins, separated by polyacrylamide gel electrophoresis, appeared identical in the three experimental groups.

Age Factors↗
PubMed2026

MNV-aware molecular characterization of a rare homozygous TTPA complex allele in ataxia with vitamin E deficiency.

Ataxia with vitamin E deficiency (AVED) is a rare autosomal-recessive neurological disorder caused by biallelic pathogenic variants in TTPA. Early vitamin E supplementation may prevent or limit irreversible neurological damage, but diagnosis is often delayed. Multi-nucleotide variants (MNVs) in TTPA have rarely been described and may be misinterpreted when adjacent substitutions are evaluated independently. We investigated a 34-year-old woman with childhood-onset progressive ataxia using clinical, biochemical, neuroimaging, and electrophysiological assessments. Serum vitamin E levels were measured longitudinally during supplementation. Whole-exome sequencing, read-level inspection, and Sanger sequencing were used to identify and confirm a homozygous TTPA complex allele, NM_000370.3:c. 296G > A;299 A > C, predicted to result in NP_000361.1:p. Gly99_Tyr100delinsAspSer, and to assess familial segregation. Population-database review, in silico prediction, and exploratory structure-based analysis were performed to evaluate its potential clinical relevance. The patient had markedly reduced baseline serum vitamin E levels of 0.8 µg/mL, which increased to 7.5 µg/mL after 12 months of supplementation. This biochemical correction was temporally accompanied by qualitatively observed improvements in gait stability, coordination, speech, and fine motor performance. Read-level analysis supported the presence of both substitutions on the same allele, and Sanger sequencing confirmed the homozygous complex allele in the patient and heterozygous carrier status in both parents. The affected residues are conserved and located within the CRAL-TRIO domain of α-tocopherol transfer protein. Exploratory structure-based analysis suggested altered local residue interactions; however, no functional assay was performed, and effects on protein stability, α-tocopherol binding, or transfer could not be established. This report expands the molecular spectrum of AVED by describing a homozygous TTPA complex allele and highlights the importance of MNV-aware interpretation of closely spaced substitutions. Vitamin E supplementation resulted in biochemical correction and was accompanied by possible partial clinical improvement despite initiation in adulthood. Functional studies are required to determine the precise effect of this allele on α-tocopherol transfer protein function.

Humans↗
PubMed1976

Selenium in in vitamin-E-deficient diets and the occurrence of myopathy as a symptom of vitamin E deficiency.

The occurrence of myopathy in vitamin-E-deficient ducklings, which is used for the determination of the degree of vitamin E deficiency, is depending on the selenium content of the diet. The selenium content of a semi-synthetic diet and its constituents was determined by neutron activation analysis, which showed to be an adequately sensitive and precise method of analysis for selenium. The casein compound was the main source of the selenium in the diet. Myopathy occurred with diets containing about 50 ppb Se; diets containing about 100 ppb Se failed to induce any signs of myopathy.

Animal Feed↗
PubMed1978

Plasma activity of pyruvate kinase and glutamic oxalacetic transaminase as indices of myopathy in the vitamin E deficient rat.

Weanling rats were fed vitamin E deficient diets for 6 to 15 weeks and then given vitamin E orally for 4 days. Plasma obtained 1 day after the last dose was assayed for glutamic oxalacetic transaminase (GOT) and pyruvate kinase activity (PK). Administration of vitamin E resulted in reduction in activity of both enzymes. Plasma levels of alkaline phosphatase, lactic dehydrogenase, and bilirubin were unaffected by vitamin E and there was no histological evidence of liver degeneration. The number of phagocytized muscle fibers was greatly reduced by vitamin E treatment, but a substantial number of necrotic fibers were still present. With more prolonged (8 days) treatment, plasma PK and GOT levels were reduced to levels found in plasma of vitamin E replete animals and few degenerated muscle fibers could be observed. It was concluded that resolution of the necrotizing myopathy in vitamin E deficient rats is a rapid process and that the decreased activity of PK and GOT in plasma is a sensitive indicator of the resolution process. The decrease in plasma enzyme levels is an easily quantitated and reproducible biological response to vitamin E administration. Thus, this approach provides a basis for a sensitive and accurate bioassay for vitamin E activity.

Animals↗
PubMedDate not supplied

Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans.

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs).

Animals↗
PubMed1977

Vitamin E deficiency and enhanced platelet function: reversal following E supplementation.

Marked platelet hyperaggregability to adenosine diphosphate, epinephrine, and collagen was demonstrated in two children with vitamin E deficiency, with complete reversal following E supplementation. No clinical thrombotic tendency was observed during the E-deficient state. The action of vitamin E in the schema of platelet arachidonate peroxidation appears to be at the step of phosphilpase A activation, or the conversion of arachidonic acid into the cyclic endoperoxides, since the peroxidation product malonaldehyde was increased during the E-deficient state with normalization following E sufficiency.

Adenosine Diphosphate↗
PubMed1975

An abnormality of the bone marrow associated with vitamin E deficiency in sheep.

1. Sheep fed on a maintenance ration of wheaten-hay chaff or of wheaten-hay chaff-lucerne-hay chaff (I : I, W/W) became deficient or incipiently deficient in vitamin E. 2. Degenerative changes were observed in bone marrow and muscle, and liver function was imparied in some animals. These abnormalities were not influenced by the vitamin B12 status of the animals or by a shortage of cobalt in the rumen. 3. Plasma ascorbic acid levels may not have been optimum, and folic may not have been fully utilized by some sheep. 4. Liver function responded faily rapidly to alpha-tocopheryl acetate, but skeletal muscle had not returned to normal after 28 weeks of treatment. A variable trend towards normal cellularity was found in bone marrow following supplementation with alpha-tocopheryl acetate. 5. A secondary deficiency or, alternatively, inefficient excretion or metabolism of a toxic material, may occur in vitamin E deficiency as a result of degenerative changes in the absorptive or excretory areas of the intestinal tract and be responsible for the bone marrow abnormality.

Animal Feed↗
PubMed1975

The effect of vitamin E deficiency on androgen and corticosterone synthesis.

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.

Adrenal Cortex↗
PubMed1977

Effects of intramuscular injections of selenium and vitamin E on selenium-vitamin E deficiency in young pigs.

Effects of intramuscular injections of selenium and vitamin E on lesions in pigs with selenium-vitamin E deficiency syndrome were determined in 2 factorial experiments, using a total 69 pigs. The pigs were fed a selenium-vitamin E deficient, 22.3% protein ration, supplemented with methionine, minerals, and vitamins. Weekly intramuscular injections of isotonic saline solution, vitamin E, selenium, or vitamin E and selenium were given to the respective treatment groups. Selenium-vitamin E deficiency lesions occurred only in pigs that were given saline injections. Weekly intramuscular injections of either selenium (as selenous acid buffered to pH (7.3) at the rate of 0.05 mg/kg of body weight or vitamin E at the rate of 20 IU/kg of body weight or the combination of selenium and vitamin E prevented cardiac and skeletal myodegeneration, hepatic necrosis, and death. Significant increases of serum aspartate aminotransferase activity values were noted in pigs with liver, heart, or skeletal muscle lesions, but these increases were not correlated with the extent of the lesions. Vascular lesions, epicardial and endocardial hemorrhages, and yellow discoloration of body fat were not features of this experimentally induced disease. These lesions may be related to factors other than the deficiency of selenium, vitamin E, or selenium and vitamin E in rations previously used in reported studies.

Animals↗
PubMed1977

Ultrastructural alterations in nutritional cardiomyopathy of selenium-vitamin E deficient swine. II. Vascular lesions.

Selenium-vitamin E deficiency was produced in weanling swine by feeding a semisynthetic basal diet for 13 to 59 days. Pigs were killed sequentially for morphologic studies of the cardiac lesions. In hearts with vascular damage, gross hemorrhages were scattered in the myocardium and serosal surfaces. Light and electron microscopic study revealed myocardial arteriolar damage characterized by segmental fibrinoid accumulation in vessel walls and by scattered fibrin thrombi. Ultrastructural study disclosed extensive subendothelial and inner wall accumulations of dense granular deposits of serum proteins and masses of fibrin in arterioles in which dense deposits of fibrinoid were identified by light microscopy. Endothelial cells of these arterioles were loosely attached to each other. In arterioles with fibrin thrombi, the endothelium was disrupted. In mildly injured arterioles, increased endothelial permeability resulted in insudation of blood proteins into the vessel wall to produce accumulation of fibrinoid. In severely injured vessels, endothelial integrity was destroyed, smooth muscle cells were necrotic and thrombosis had developed. Initiation of these arteriolar lesions was apparently the result of lipoperoxidative damage to endothelial cell membranes that lacked protection by selenium-vitamin E.

Animals↗
PubMed1977

The anemia of vitamin E deficiency in swine: an experimental model of the human congenital dyserythropoietic anemias.

The ultrastructural and erythrokinetic characteristics of vitamin E deficiency in swine were investigated in an effort to evaluate the suitability of the swine disorder as a model of the human congenital dyserythropoietic anemias. The dominant erythrokinetic abnormality in vitamin E deficient pigs, as in the CDAs, is ineffective erythropoiesis. As in some patients with CDA, the activity of a number of erythrocyte enzymes was increased. Distinctive ultrastructual changes previously described in patients with CDA were found in normoblasts from vitamin E deficient pigs. The morphologic, erythrokinetic, biochemical and ultrastructural similarities between vitamin E deficiency in swine and the CDAs in man appear to justify the study of the animal disorder as a model of the human disease. A complete hematologic response was elicited by the administration not only of vitamin E, but also, as in the previous studies of vitamin E deficiency in monkeys, by hexahydrocoenzyme Q4. The partial hematologic response occurring after deletion of tocopherol stripped corn oil from the diet indicates that factors other than the dietary lack of vitamin E are important in the pathogenesis of this disorder.

Anemia↗
PubMed1978

Possible interrelationship between vitamins E and b12 in the disturbance in methylmalonate metabolism in vitamin E deficiency.

1. The disturbance in 2-methylmalonate metabolism resulting in its increased urinary excretion observed in vitamin E deficiency is not caused by increased formation of methylmalonate from propionate as is evident from the activity of the enzyme propionyl-CoA carboxylase (EC 6.4.1.3), but can be traced to an impairment in the conversion of methylmalonate into succinate by the vitamin B12-requiring enzyme, methylmalonyl-CoA mutase (EC 5.4.99.2) in rat liver. 2. It is shown that the decrease in the activity of methylmalonyl-CoA mutase in vitamin E deficiency is not a consequence of a secondary vitamin B12 deficiency. Peroxidative destruction of the coenzyme in vitamin E deficiency was also ruled out. The results suggest a defect in the conversion of cyanocobalamin into its coenzyme form.

Animals↗
PubMed1975

The effects of vitamin E deficiency on some enzymes of steroid hormone biosynthesis.

The effect of vitamin E deficiency on three enzyme systems involved in steroidogenesis was investigated. No change was found in vitro activity of cholesterol side-chain cleavage enzyme in adrenal or testicular tissue, or of 11-beta-hydroxylase activity in adrenal tissue. Significantly less 3-beta-hydroxysteroid dehydrogenase activity was found in ovarian tissue from female rats given a diet deficient in vitamin E for 141 days, and in testicular tissue and adrenal glands from male rats given the deficient diet for 280 days. Testicular tissue from male rats given the deficient diet for 91 days showed considerably less 3-beta-hydroxysteroid dehydrogenase activity than did tissue from control rats, but the difference was not statistically significant.

Adrenal Glands↗
PubMed1975

Depression of lecithin-cholesterol acyltransferase esterification in vitamin E-deficient monkeys.

Vitamin E deficiency in two species of monkeys (capuchins and cynamolgus) reduced the in vitro cholesterol esterification by plasma lecithin-cholesterol acyltransferase. The reduction was greates in the most deficient species and in animals fed a diet rich in polyunsaturated fat (safflower oil) stripped of vitamin E. The best correlate of total esterification was the plasma concentration of free cholesterol which reflected the degree of hyperlipidemia, found to be greatest in capuchins fed coconut oil. A logical explanation for the decreased LCAT activity in vitamin E deficiency would be peroxidative damage of substrate (the PUFA of lecithin) or of sulfhydryl sited on lecithin-cholesterol acyltransferase itself. However, neither case was fully supported by the data suggesting that additional information concerning the nature of the reaction and the role of vitamin E is required.

Acyltransferases↗
PubMed1975

Purification and characterization of xanthine oxidase from livers of vitamin E deficient rabbits.

Xanthine oxidase which increases in activity during vitamin E deficiency was purified from livers of deficient rabbits. The procedure incorporates preparative sucrose gradient centrifugation and yields a homogeneous preparation on acrylamide gel electrophoresis. The purified enzyme exhibits a pH optimum of 8.1 and a Km value of 22 muM. Gel filtration chromatography gave the molecular weight of 280 000. Acrylamide gel electrophoresis in the presence of sodium dodecylsulphate reveals two types of subunits of molecular weights 52 000 and 99 000.

Animals↗