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At least 19 recordsLinked to original sources
PubMed1997

Neurologic findings in vitamin E deficiency.

Vitamin E is one of the most important lipid-soluble antioxidant nutrients. Severe vitamin E deficiency can have a profound effect on the central nervous system. Cystic fibrosis, chronic cholestatic liver disease, abetalipoproteinemia, short bowel syndrome, isolated vitamin E deficiency syndrome and other malabsorption syndromes all may cause varying degrees of neurologic deficits due to related vitamin deficiencies. The classic abnormalities in vitamin E deficiency progress from hyporeflexia, ataxia, limitations in upward gaze and strabismus to long-tract defects, profound muscle weakness and visual field constriction. Patients with severe, prolonged deficiency may develop complete blindness, dementia and cardiac arrhythmias. Treatment must be tailored to the underlying cause of vitamin E deficiency and may include oral or parenteral vitamin supplementation. The more advanced the deficits, the more limited the response to therapy. Therefore, a good neurologic examination and periodic serum vitamin E levels are essential in patients at risk of vitamin E deficiency.

Adult↗
PubMed2001

Immunological dysregulation of lung cells in response to vitamin E deficiency.

Vitamin E supplementation exhibits anti-inflammatory properties. In the lung, the beneficial effects of vitamin E supplementation on inflammation and infections are well documented, but potential consequences of alimentary vitamin E deficiency to the immunological status of lung cells are not known. It is unclear if temporary vitamin E deficiency exhibits deleterious consequences or can be compensated for by other cellular antioxidants. To address this question, the alimentary vitamin E supply to rats was modified. We then investigated the effects on major histocompatibility molecule (MHC) class II, cell adhesion molecules, interleukin (IL)10, tumor necrosis factor (TNF)alpha in various lung cells. The constitutive expression of MHC class II, intercellular adhesion molecule (ICAM)-1, L-selectin, alpha5-integrin, and CD 166, was demonstrated by flow cytometry on type II pneumocytes, alveolar macrophages, and on co-isolated lymphocytes. Vitamin E depletion increased ICAM-1 and CD166 on type II cells and macrophages, whereas the expression of L-selectin increased only on macrophages. Furthermore, the vitamin E depletion increased the cellular content and secretion of IL10 in type II cells, but decreased the content and secretion of TNFalpha. Vitamin E depletion decreased the cellular vitamin E content, but did not change the activity of antioxidant enzymes (catalase, superoxide dismutase) and the glutathion (GSH)/oxidized glutathion (GSSG) ratio in alveolar type II cells. The shift of protein kinase C (PKC) from the cytosol to membranes indicates that a PKC-dependent signaling pathway may be involved in the change of the immunological status of type II cells. All these effects were reversed by vitamin E repletion. In summary, these results are clearly compatible with the view that a temporary vitamin E deficiency induces a reversible immunological dysregulation in alveolar type II cells and lung macrophages. This deficiency might predispose the lung to develop acute or chronic inflammation.

Animals↗
PubMedDate not supplied

[Chronic polyneuropathy due to vitamin E deficiency].

Vitamin E deficiency has been implicated as a causal factor in neurological disease for some time. Nevertheless, only in the last 10 years have we begun to understand the role this vitamin plays in the normal functioning and structure of the nervous system. Chronic fat malabsorption syndromes are the most common causes of low levels of this highly fat-soluble vitamin. We present a case of chronic polyneuropathy due to vitamin E deficiency caused by malabsorption in which a biliary-cholonic fistula was present. Plasma tocopherol levels were normalized by parenteral substitution, leading to substantial clinical improvement. We suggest that vitamin E levels be determined in cases of digestive disorders involving malabsorption of fats and in chronic neurological diseases, particularly spinal-cerebral degenerative and polyneuropathic diseases that are mainly sensory or motor-sensory in nature, given the potential reversibility of these disorders when caused by vitamin E deficiency.

Female↗
PubMed1994

Modulation of rat heart mitochondrial function and the production of reactive oxygen by vitamin E deficiency.

Vitamin E, an antioxidant present in all cellular membranes, is associated with protein complexes in the inner mitochondrial membranes and may affect oxidative changes which occur in these organelles when heart tissue is subjected to hypoxia. The effect of 60 min hypoxia, after a 30 min normoxic equilibration period, on the function and the production of reactive oxygen species (ROS) by cardiac mitochondria from rats fed vitamin E sufficient or deficient diets for 9 weeks was examined. Mitochondria from the hearts of rats fed vitamin E deficient diets had 40-fold less vitamin E and were more susceptible to lipid peroxidation, as compared to heart mitochondria from rats fed vitamin E sufficient diet. Perfusion with normoxic, but not hypoxic, media significantly decreased cardiac vitamin E in deficient, but not sufficient rats. Hypoxia decreased the production of ROS by mitochondria from vitamin E sufficient hearts, compared to normoxia. A similar level of ROS production was seen after hypoxia in mitochondria from vitamin E deficient hearts. However, vitamin E deficiency alone decreased the production of ROS by mitochondria from normoxic hearts, relative to vitamin E sufficient animals. Under all conditions where the production of ROS was decreased, 1 microM calcium increased production to the maximum levels seen in vitamin E sufficient, normoxic heart mitochondria. Mitochondrial function was depressed in mitochondria from hypoxic hearts as compared to mitochondria from normoxic hearts of vitamin E sufficient rats. A similar depression of mitochondrial function was not seen in mitochondria from hypoxic hearts of vitamin E deficient rats. Compensatory changes in response to long-term vitamin E deficiency may be responsible for the differences in response to hypoxia of mitochondria from vitamin E sufficient and deficient rats.

Animals↗
PubMed2006

Protective effect of vitamin E supplements on experimental atherosclerosis is modest and depends on preexisting vitamin E deficiency.

Vitamin E has failed to protect humans from cardiovascular disease outcome, yet its role in experimental atherosclerosis remains less clear. A previous study (Proc. Natl. Acad. Sci. USA 97:13830-13834; 2000) showed that vitamin E deficiency caused by disruption of the alpha-tocopherol transfer protein gene (Ttpa) is associated with a modest increase in atherosclerosis in apolipoprotein E gene deficient (Apoe(-/-)) mice. Here we confirm this finding and report that in Apoe(-/-)Ttpa(-/-) mice dietary alpha-tocopherol (alphaT) supplements restored circulating and aortic levels of alphaT, and decreased atherosclerosis in the aortic root to a level comparable to that seen in Apoe(-/-) mice. However, such dietary supplements did not decrease disease in Apoe(-/-) mice, whereas dietary supplements with a synthetic vitamin E analog (BO-653), either alone or in combination with alphaT, decreased atherosclerosis in Apoe(-/-) and in Apoe(-/-)Ttpa(-/-) mice. Differences in atherosclerosis were not associated with changes in the arterial concentrations of F(2)-isoprostanes and cholesterylester hydro(pero)xides, nor were they reflected in the resistance of plasma lipids to ex vivo oxidation. These results show that vitamin E at best has a modest effect on experimental atherosclerosis in hyperlipidemic mice, and only in situations of severe vitamin E deficiency and independent of lipid oxidation in the vessel wall.

Animals↗
PubMed2006

Differential gene expression in skeletal muscle of rats with vitamin E deficiency.

Vitamin E (VE) deficiency is accompanied by myopathy in various animal species including man. Although gene expression profiles related to degenerative and regenerative processes in different kinds of myopathies have been studied, no global expression profile for skeletal muscle subject to VE deficiency has previously been reported. In the present study, Affymetrix GeneChip technology was used to obtain such a profile. Two groups of male rats were fed with either a diet deficient in VE or a control diet. Differential gene expression was monitored at five time-points over 430 days, with all animals individually profiled. Out of approximately 7000 genes represented on the Genechip, 56 were found to be up-regulated in response to VE deficiency in at least four consecutive time-points from as early as 91 days of deficiency. Up-regulated genes included muscle structure and extra cellular matrix genes, as well as anti-oxidative, anti-inflammatory and anti-fibrotic genes. Our data show that molecular transcription might provide a very early marker to detect oncoming degenerative conditions in VE deficiency. They provide further insight into possible molecular mechanisms underlying VE deficiency in skeletal muscle, and reveal the activation of an intensive protection program that can explain the long maintenance of muscle structure during deficiency.

Animals↗
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↗
PubMed1982

Effect of selenium deficiency and vitamin E deficiency on glutathione metabolism in isolated rat hepatocytes.

Selenium deficiency and vitamin E deficiency both affect xenobiotic metabolism and toxicity. In addition, selenium deficiency causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione metabolism in isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during the 5-h incubation. Freshly isolated hepatocytes had the same glutathione concentration regardless of diet group. During the incubation, however, the glutathione concentration in selenium-deficient hepatocytes rose to 1.4 times that in control hepatocytes. The selenium-deficient cells also released twice as much glutathione into the incubation medium as did the control cells. Total glutathione (intracellular plus extracellular) in the incubation flask increased from 47.7 +/- 8.9 to 152 +/- 16.5 nmol/10(6) selenium-deficient cells over 5 h compared with an increase from 46.7 +/- 7.1 to 92.0 +/- 17.4 nmol/10(6) control cells and from 47.7 +/- 11.7 to 79.5 +/- 24.9 nmol/10(6) vitamin E-deficient cells. This overall increase in glutathione concentration suggested that glutathione synthesis was accelerated by selenium deficiency. The activity of gamma-glutamylcysteine synthetase was twice as great in selenium-deficient liver supernatant (105,000 X g) as in vitamin E-deficient or control liver supernatant (105,000 X g). Hemoglobin-free perfused livers were used to determine the form of glutathione released and its route. Selenium-deficient livers released 4 times as much GSH into the caval perfusate as did control livers. Plasma glutathione concentration in selenium-deficient rats was found to be 2-fold that in control rats, suggesting that increased GSH synthesis and release is an in vivo phenomenon associated with selenium deficiency.

Animals↗
PubMed1986

Vitamin E deficiency and vitamin C supplements: exercise and mitochondrial oxidation.

The effects of dietary antioxidant vitamins E and C on exercise endurance capacity and mitochondrial oxidation were investigated in rats. The endurance capacity of both vitamin E-deficient and vitamin C-supplemented, E-deficient rats was significantly (P less than 0.05) lower (38.1 and 33.6%, respectively) than control animals. Compared with the normal and vitamin E-deficient rats, there was a significant (P less than 0.05) increase in the concentration of vitamin C in blood and liver of the vitamin E-deficient, C-supplemented animals. Hence dietary vitamin C supplementation does not prevent the inhibition of exercise endurance capacity or increased hemolysis seen in vitamin E deficiency. The mitochondrial activities for the oxidation of palmitoyl carnitine and alpha-ketoglutarate were significantly (P less than 0.05) decreased by a single bout of exercise in brown adipose tissue but not in muscle, heart, or liver from vitamin C-supplemented, E-deficient groups of rats when compared with the activities in the tissue from the same group of rats killed at rest. Similar results were also seen in brown adipose tissue from vitamin E-deficient rats. The results suggest a tissue-specific role for vitamins E and C in substrate oxidation and show that the poor endurance capacity of vitamin E-deficient rats cannot be attributed to any changes in the mitochondrial activity in skeletal or cardiac muscles. It is also concluded that vitamin C supplementation, at least at the dose employed in the present study, cannot counteract the detrimental effects associated with vitamin E deficiency.

Adipose Tissue, Brown↗
PubMed1996

Disappearance of skin lipofuscin storage and marked clinical improvement in adult onset coeliac disease and severe vitamin E deficiency after chronic vitamin E megatherapy.

A case of adult onset coeliac disease with IgA and severe vitamin E deficiencies, associated with cerebellar impairment and peripheral neuropathy, is described. Nerve conduction velocities, BAERs and SEP were altered. Brain nMR showed cortical atrophy mainly in the frontal and parietal regions. At ultrastructural examination, nerve biopsy showed a severe nerve fiber loss with presence of lipofuscin. Lipofuscin has been also found in skin and muscle biopsy. Duodenal biopsy showed villar atrophy with criptae hypoplasia. IgA, Apo A1 lipoprotein and cholesterol were decreased. Serum level of vitamin E was not detectable and its amount did not increase after an oral loading (2 g bolus). Parenteral vitamin E administration (900 mg/day) was able to normalize the plasma values only after 6 months of chronic administration of the drug in coincidence with a significant improvement of clinical and neurophysiological signs, and disappearance of lipofuscin storage in the skin biopsy.

Brain Diseases, Metabolic↗
PubMed2004

Vitamin E deficiency induced neurological disease in common variable immunodeficiency: two cases and a review of the literature of vitamin E deficiency.

Vitamin E deficiency causes a neurological disorder characterised by sensory loss, ataxia and retinitis pigmentosa due to free radical mediated neuronal damage. Symptomatic vitamin E deficiency has been reported in genetic defects of the vitamin E transport protein and in malabsorption complicating cholestasis, abetalipoproteinaemia, celiac disease, cystic fibrosis and small bowel resection. There are no reports to date of vitamin E deficiency in patients with primary immunodeficiencies. We describe two CVID patients with the associated enteropathy who developed neurological disease because of vitamin E deficiency, suggesting a possible predisposition to developing this complication. We recommend that all CVID patients with evidence of an enteropathy be screened for vitamin E deficiency, as early detection and consequent treatment may prevent, halt or reverse the neurological sequelae.

Adult↗
PubMed1996

Human alpha-tocopherol transfer protein: gene structure and mutations in familial vitamin E deficiency.

Familial vitamin E deficiency (AVED) causes ataxia and peripheral neuropathy that resembles Friedreich's ataxia. AVED is thought to be caused by a defect in the transport of vitamin E in liver cells, which is the probable function of alpha-tocopherol transfer protein (alphaTTP). We have cloned the cDNA and several genomic phage clones covering the entire human alphaTTP gene and determined the junctions between the five exons and four introns that composed the gene for human alphaTTP. Three mutations in three unrelated North American families with AVED were identified. Two mutations, 485delT and 513insTT, cause a frame shift and a premature stop codon and the third mutation 574G-->A would substitute Arg192 to His in alphaTTP. The 2 patients with a severe form of AVED were homozygous with 485delT and 513insTT, respectively, while the patient with a mild form of the disease was compound heterozygous with 513insTT and 574G-->A. These findings have identified the underlying genetic defect in AVED and have confirmed the role of alphaTTP in AVED.

Adolescent↗
PubMed1984

Vitamin E deficiency with normal serum vitamin E concentrations in children with chronic cholestasis.

We studied serum vitamin E levels and the ratio of serum vitamin E to serum lipid levels in 11 children with chronic cholestasis complicated by vitamin E deficiency, as defined by characteristic neurologic signs or sural-nerve histopathology in addition to impaired intestinal absorption of vitamin E. Eight of the children had low levels of serum vitamin E, as well as low ratios of serum vitamin E to total lipids and to cholesterol. However, three patients had normal serum vitamin E levels but low ratios of serum vitamin E to total lipids (two of the three had normal ratios of vitamin E to cholesterol). In four patients who were not vitamin E-deficient, all three values were normal. We conclude that vitamin E deficiency may exist in a child with a normal serum vitamin E concentration and that the ratio of serum vitamin E to total serum lipids is the most reliable biochemical index of vitamin E status during chronic childhood cholestasis.

Adult↗
PubMedDate not supplied

[Electro-oculographic features of persons with vitamin E deficiency].

INTRODUCTION: Vitamin E (VE) deficiency is a very rare condition which may be due to an isolated deficit or be in the context of a malabsorption disorder. OBJECTIVE: To evaluate the findings from an electrooculographic (EOG) point of view of patients with VE deficiency. PATIENTS AND METHODS: We made a retrospective evaluation of all persons with a neurological diagnosis of VE seen in the otoneurological department of our hospital. In all patients an EOG recording was made of the saccadic jerks, and the spontaneous, provoked, positional and opticokinetic (NOC) mystagmus, visual suppression of the vestibulo ocular reflex (VOR) and follow up. RESULTS: We found four cases, with an average age of 9.2 years (range 6 14 years). All the patients but one were male (75%). The EOG findings were related to cerebellar dysfunction (saccadic following) and central nervous system alterations of no value for localization (ataxic following and visual suppression of the VOR). In two patients no anomalies were seen on the EOG recording. CONCLUSIONS: In persons with VE deficiency EOG alterations are not often seen. However, it may be useful to make the recording when it is thought necessary to detect subclinical cerebellar disorders.

Adolescent↗
PubMed1995

[Neurological symptoms associated with vitamin E deficiency].

Children deficient in vitamin E have various neurologic symptoms. 2 cases representing different mechanisms of this vitamin deficiency are reported. A 15-year-old boy with fat malabsorption due to cystic fibrosis who was diagnosed as being vitamin E deficient (< 0.5 mg/l), had typical neuropathies. On the other hand, a 12-year-old Beduin girl had isolated vitamin E deficiency, as well as neurological symptoms suggestive of Friedrich's ataxia. Vitamin E supplementation by intramuscular injection in the first case and per os in the second led to significant improvement in neurological symptoms.

Adolescent↗