Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrosis and apoptosis coexist in the thyroid during goitre development and involution, but little is known about their respective causes. To test the possible role of free radicals, we analysed separately necrosis and apoptosis in male Wistar rats with depressed or normal antioxidant protection. Vitamin E-deficient and -sufficient rats were made goitrous with perchlorate in drinking water; involution was induced by repeated injection of NaI, without or with methimazole. Increase of thyroid malondialdehyde concentration and decrease of glutathione peroxidase activity confirmed the depressed antioxidant protection in vitamin E-deficient rats. Plasma thyroxine and TSH levels were not modified. Necrosis (swollen cells) and apoptosis (pyknotic cells) were quantified on histological sections. In vitamin E-sufficient rats, dead cells were very rare in control thyroids, increased 3-fold in goitre and still further during involution. Necrotic epithelial cells predominated in the goitre and their number declined after iodide supplementation, without or with methimazole. In contrast, the number of apoptotic cells and the caspase-3 activity were increased in goitre and further increased after involution, with two-thirds of pyknotic cells being observed in the interstitium. Apoptosis was prevented by methimazole. Vitamin E deficiency significantly increased total cell death and epithelial cell necrosis and induced the occurrence of much cell debris in the follicular lumen during involution, with no modification of the apoptotic reaction. These results show that the type of cell death is differentially regulated during goitre development and involution: necrosis is related to the oxidative status of the cells, while apoptosis comes with iodine-induced involution.
 ...
PMID:Cell necrosis and apoptosis are differentially regulated during goitre development and iodine-induced involution. 1183 55

Vitamin E is a generic term denoting eight different isomers among which alpha-tocopherol is the most important and most active. Vitamin E metabolism is closely linked to lipids during intestinal absorption, plasma secretion and transport, and tissue uptake. It is a key compound involved in many physiological processes, such as neurological and immune functions. The most common role of vitamin E is its antioxidant effect, protecting molecules and tissues against the deleterious effect of free radicals. Vitamin E also contributes to the stabilization of biological membranes. In addition, it intervenes in the regulation of several enzymes and probably has impact on gene expression. Advancing knowledge about vitamin E has been achieved with high performance liquid chromatography, making assay accessible to many laboratories, and the use of deuterated derivatives to better apprehend its metabolism. Certain issues remain unresolved concerning the molecular basis of vitamin E's mechanism of action and the exact nature of metabolic dysfunction leading to the clinical manifestations of severe vitamin E deficiency.
 ...
PMID:[Vitamin E: structure, metabolism, and functions]. 1190 51

Pre-term neonates and neonates in general exhibit physiological vitamin E deficiency and are at increased risk for the development of acute lung diseases. Apoptosis is a major cause of acute lung damage in alveolar type II cells. In this paper, we evaluated the hypothesis that vitamin E deficiency predisposes alveolar type II cells to apoptosis. Therefore, we measured markers of apoptosis in alveolar type II cells isolated from control rats, vitamin E deficient rats and deficient rats that were re-fed a vitamin E-enriched diet. Bax and cytosolic cytochrome c increased, and the mitochondrial transmembrane potential and Hsp25 expression was reduced in vitamin E deficiency. Furthermore, increased DNA-fragmentation and numbers of early and late apoptotic cells were seen, but caspases 3 and 8 activities and expression of Fas, Bcl-2, Bcl-x and p53 remained unchanged. Vitamin E depletion did not change the GSH/GSSG ratio and the activities of antioxidant enzymes. Thus, vitamin E deficiency may induce a reversible pro-apoptotic response in lung cells and sensitise them for additional insult. In agreement with this hypothesis, we demonstrate that in vivo hyperoxia alone does not induce apoptosis in type II cells of control rats but reversibly increases DNA-fragmentation and numbers of early apoptotic type II cells in vitamin E-depleted cells.
 ...
PMID:Vitamin E deficiency sensitizes alveolar type II cells for apoptosis. 1206 53

Alveolar type II cells accumulate vitamin E preferentially from high-density lipoproteins (HDL) and express at least three receptors that are specific for HDL. The expression of these receptors increases in response to vitamin E deficiency. Beside receptors for specific lipid transfer from HDL, cubilin and megalin, several other receptors that mediate HDL-particle uptake were found in the lung. We hypothesize that alveolar type II cells also exhibit the HDL-particle uptake and that this process can be regulated by the vitamin E status. By confocal laser microscopy and flow cytometry we showed that type II cells accumulate protein-labeled HDL-particle. Vitamin E depletion in rats increased HDL-particle uptake in alveolar type II cells and the expression of megalin. The expression of cubilin did not change. Refeeding with vitamin E reversed HDL-particle uptake and megalin expression. Long-time incubation of type II cells with phorbol myristyl acetate (PMA) reduced HDL-holoparticle uptake and megalin expression. We assume that alveolar type II cells exhibit HDL-holoparticle uptake mediated by megalin and cubilin. Megalin represents the regulated element of the megalin/cubilin receptor-cooperation and can be modulated by protein kinase C.
 ...
PMID:HDL-holoparticle uptake by alveolar type II cells: effect of vitamin E status. 1209 Dec 46

We describe a young patient affected by vitamin E deficiency with mutation in the tocopherol transfer protein alleles and the unique presentation as myoclonic dystonia, which was practically the only symptom for 6 years before ataxia became evident. Vitamin E supplementation markedly improved both symptoms. This unusual clinical phenotype must be considered, because isolated vitamin E deficiency is eminently treatable.
 ...
PMID:Myoclonic dystonia as unique presentation of isolated vitamin E deficiency in a young patient. 1211 20

In this study the effects of vitamin E deficiency and supplementation on bone calcification were determined using 4-month-old female Sprague-Dawley rats. The rats weighed between 180 and 200 g. The study was divided in three parts. In experiment I the rats were given normal rat chow (RC, control group), a vitamin E deficient (VED) diet or a 50% vitamin E deficient (50%VED) diet. In experiment 2 the rats were given VED supplemented with 30 mg/kg palm vitamin E (PVE30), 60 mg/kg palm vitamin E (PVE60) or 30 mg/kg pure alpha-tocopherol (ATF). In experiment 3 the rats were fed RC and given the same supplements as in experiment 2. The treatment lasted 8 months. Vitamin E derived from palm oil contained a mixture of ATF and tocotrienols. Rats on the VED and 50%VED diets had lower bone calcium content in the left femur compared to the RC group (91.6 +/- 13.3 mg and 118.3 +/- 26.0 mg cf 165.7 +/- 15.2 mg; P < 0.05) and L5 vertebra (28.3 +/- 4.0 mg and 39.5 +/- 6.2 mg compared with 51.4 +/- 5.8 mg; P < 0.05). Supplementing the VED group with PVE60 improved bone calcification in the left femur (133.6 +/- 5.0 mg compared with 91.6 +/- 13.3 mg; P < 0.05) and L5 vertebra (41.3 +/- 3.3 mg compared with 28.3 +/- 4.0 mg; P < 0.05) while supplementation with PVE30 improved bone calcium content in the L5 vertebra (35.6 +/- 3.1 mg compared with 28.3 +/- 4.0 mg; P < 0.05). However, supplementation with ATF did not change the lumbar and femoral bone calcium content compared to the VED group. Supplementing the RC group with PVE30, PVE60 or ATF did not cause any significant changes in bone calcium content. In conclusion, vitamin E deficiency impaired bone calcification. Supplementation with the higher dose of palm vitamin E improved bone calcium content, but supplementation with pure ATF alone did not. This effect may be attributed to the tocotrienol content of palm vitamin E. Therefore, tocotrienols play an important role in bone calcification.
 ...
PMID:Tocotrienols are needed for normal bone calcification in growing female rats. 1223 Feb 32

This review of the nutritional needs of very low birth weight infants (VLBW) concluded that vitamin supplementation was indicated for vitamins A, D, C, and folic acid. With breast feeding or other circumstances, there may be marginal needs for vitamin E, K, B1, B2, and B6. Supplementation of VLBW depends upon the gestation age, which is related to the placental transfer and body stores at birth, and vitamin content of breast milk or formula (feeds), and volume and micronutrient composition of feeds. The infant's vitamin stores at birth are dependent on the nutritional status of the mother, particularly lipid soluble vitamins, which have been found to be higher in fetal cord blood than in maternal blood. The exception is B6, which crosses the placental barrier with difficulty. Preterm infants and infants of undernourished mothers usually have reduced levels of water soluble vitamins at birth. There is some variability in nutrients of feeds. Breast milk, for instance, has lower levels of vitamins D and K than recommended levels. Needs will also very with the presence of particular nutrients. For example, B6 requirements will vary with protein intake. Vitamin E requirements will depend on the amount of linoleic acid or polyunsaturated fatty acids in the diet. Tryptophan in the presence of B6 allows the synthesis of niacin. Volume of feeding affects nutritional needs. The recommended daily allowance (RDA) of specific nutrients for an infant up to 6 month of age and weighing 3-8 kg requires consumption of 500-1000 ml of breast milk or formula per day. A full term infant can receive sufficient nutrients with 450-750 ml, but below 400 would result in a deficit of vitamins. Unfortunately, the volume of feeds for VLBWs is too low in the first two weeks of life or until the body weight of 2000 g is reached; thus supplementation was recommended. Late anemia due to vitamin E deficiency may be prevented when the alpha tocopherol per gram of polyunsaturated fatty acids ratio is equal to or higher than the recommended levels. When intake of vitamin K at birth is insufficient, deficiencies may appear later; the recommendation was .2 to 1.0 mg at birth as a preventive regimen. Vitamin D was also recommended for both breast and formula fed infants. Pyridoxine/ g protein intake, folic acid, and vitamin C should be provided VLBW infants as indicated.
 ...
PMID:Vitamin requirements of very low birth weight infants: a review. 1231 6

Vitamin E is indispensible for reproduction in female rats. In humans, vitamin E deficiency primarily causes neurologic dysfunctions, but the underlying molecular mechanisms are unclear. Because of its antioxidative properties, vitamin E is believed to help prevent diseases associated with oxidative stress, such as cardiovascular disease, cancer, chronic inflammation, and neurologic disorders. However, recent clinical trials undertaken to prove this hypothesis failed to verify a consistent benefit. Given these findings, a group of European scientists met to analyze the most recent knowledge of vitamin E function and metabolism. An overview of their discussions is presented in this article, which includes considerations of the mechanisms of absorption, distribution, and metabolism of different forms of vitamin E, including the alpha-tocopherol transfer protein and alpha-tocopherol-associated proteins; the mechanism of tocopherol side-chain degradation and its putative interaction with drug metabolism; the usefulness of tocopherol metabolites as biomarkers; and the novel mechanisms of the antiatherosclerotic and anticarcinogenic properties of vitamin E, which involve modulation of cellular signaling, transcriptional regulation, and induction of apoptosis. Clinical trials were analyzed on the basis of the selection of subjects, the stage of disease, and the mode of intake, dosage, and chemical form of vitamin E. In addition, the scarce knowledge on the role of vitamin E in reproduction was summarized. In conclusion, the scientists agreed that the functions of vitamin E were underestimated if one considered only its antioxidative properties. Future research on this essential vitamin should focus on what makes it essential for humans, why the body apparently utilizes alpha-tocopherol preferentially, and what functions other forms of vitamin E have.
 ...
PMID:The European perspective on vitamin E: current knowledge and future research. 1232 81

Vitamin E is thought to be involved in many essential processes in plants, but no functional proof has been reported. To study vitamin E deficiency in plants, a high-throughput biochemical screen for vitamin E quantification in Arabidopsis mutants has been developed, which has led to the identification of VTE1-encoding tocopherol cyclase. Interestingly, the corresponding maize mutation, sxd1, causes plasmodesmata malfunction, suggesting a link between tocopherol cyclase and plasmodesmata function.
 ...
PMID:Vitamin E biosynthesis: biochemistry meets cell biology. 1252 93

Increased intake of vitamin E has been suggested to be protective against prostate cancer in men, but the effects of vitamin E on prostate growth and function remain poorly defined. The purpose of this study was to determine the effects of vitamin E deficiency on pubertal growth and maturation of the prostate in the rat. Animals were placed on a vitamin E deficient diet at 28 days of age and were followed for 15 and 26 weeks. Vitamin E deficient rats had a circulating vitamin E level of less than 1% of control animals and experienced a decrease in body and testis weight. The deficiency did not alter the weights of the ventral and dorsal lobes of the prostate. However, there was an increase in weight, DNA, and protein contents of the lateral lobe in control and vitamin E deficient rats from 15 to 26 weeks of treatment, but these increases were significantly lower in vitamin E deficient 26-week treated rats. The volume of secretion per milligram tissue was greater in the ventral than lateral or dorsal lobes. The volume of secretion and activity of the secretory 26 kDa protease in the ventral prostate was lower in vitamin E deficient rats at 15 weeks, but not at 26 weeks of treatment. In contrast, the relative protein content of lateral lobe secretion increased in both control and vitamin E deficient rats from 15 to 26 weeks of treatment. The lateral, but not ventral or dorsal, lobes of both control and vitamin E deficient rats were affected by chronic prostatitis as evidenced by infiltration of inflammatory cells. The lateral lobes also showed markedly elevated activities of the matrix metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9). These data indicate that vitamin E deficiency does not alter the growth of the prostatic lobes, nor the onset and extent of lateral lobe specific prostatitis, but it may delay some differentiated functions such as secretion of specific proteins in the ventral lobe. Thus, the effects of vitamin E in the prostate of the rat appear to be selective.
 ...
PMID:Effect of vitamin E deficiency on the growth and secretory function of the rat prostatic complex. 1278 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>