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

The toxicity of ozone is solely due to its action as an oxidant. It is an extremely reactive gas which rapidly forms intermediate oxidizing derivatives after inhalation. High concentrations cause death from pulmonary oedema. Both pulmonary and extrapulmonary toxicity have been observed at lower concentrations of ozone, including those currently present in urban air. Pulmonary cellular and subcellular membranes appear to be particularly susceptible. A primary mechanism of this effect is the oxidative decomposition of polyunsaturated fatty acids, which has been demonstrated in rodent lungs after inhalation of ozone. Supporting evidence includes the potentiation of ozone toxicity by vitamin E deficiency and an increased use of this antioxidant vitamin during repetitive exposure to ozone. Other membrane effects include oxidation of thiol groups and, perhaps, of tryptophan. Microsomal alterations include a loss of lung cytochrome P450 which may also be related to lipid peroxidation. Extrapulmonary toxicity is not directly due to ozone but may represent in effect due to lipid peroxide decomposition products, particularly malonaldehyde. This three-carbon dialdehyde has been shown to alter cell membrane fluidity and to have mutagenic properties; the latter perhaps due to cross-linkage of DNA to histone.
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PMID:The pulmonary and extrapulmonary effects of ozone. 25 63

The present paper describes the identification of two vitamin E-dependent, water soluble fluorescent compounds in mouse tissues. Ultraviolet and fluorescent spectroscopy, derivatization with 1-dimethylamino-naphthalene-5-sulfonyl chloride (dansyl chloride) and cochromatography using high performance liquid chromatography (HPLC) were utilized for the identification of the unknown compounds. The water soluble fluorescent compounds in mouse tissues were identified as tyrosine and tryptophan. The compounds were previously found to increase significantly in vitamin E deficiency in various tissues.
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PMID:Identification of vitamin E-dependent water soluble fluorescent compounds in mouse tissues. 232 6

The effects of a vitamin E deficiency diet for 15 days on amino acid concentrations have been studied in the substantia nigra, striatum and hippocampus of the rat. The substantia nigra showed an increase in glutamate and GABA and a decrease of tryptophan concentration compared with controls. In the striatum, aspartate and glycine decreased, no changes were found in the amino acid concentrations in the hippocampus. The substantia nigra and striatum showed opposite results-an increase and decrease of amino acids respectively. The increase of glutamate found in substantia nigra is particularly interesting as it may suggest possible links to degenerative processes. These results suggest that vitamin E could play a crucial role in substantia nigra degeneration and that the substantia nigra could be more sensitive to an oxidative stress than other brain structures.
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PMID:The effect of a vitamin E-deficient diet on amino acid levels in the substantia nigra, striatum and hippocampus of rats. 828 99

We investigated the effects of vitamin E deficiency on the monoamine metabolism in the rat brain. Male Wistar rats fed on the vitamin E deficient diet for 24 weeks were analyzed. At 28 weeks, they showed a reduced growth rate (52% of reduction), muscle atrophy, a motor weakness of hind limbs and disturbance of gait. The concentrations of monoamines, their precursors and metabolites in the brain were simultaneously determined using high performance liquid chromatography (HPLC) coupled with a coulometric detection with electrode array system. In addition, tryptophan hydroxylase activity was measured. The dopamine (p = 0.009) and serotonin (p = 0.04) levels in the brain stem of vitamin E deficient rats were significantly lower than in the controls, whereas their precursors tyrosine (p = 0.0009) and tryptophan (p = 0.0065) levels in the brain stem were significantly higher than in the controls. Moreover, tryptophan hydroxylase activity (p = 0.0005) in the brain stem of vitamin E deficient brains was significantly lower than in the controls. All statistical comparisons were done using non-parametric tests (Mann-Whitney U test). These results suggest that vitamin E deficiency may play a role in the disturbance of monoamine metabolism in rat brain.
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PMID:Effect of vitamin E deficiency on rat brain monoamine metabolism. 1049 27

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.
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PMID:Vitamin requirements of very low birth weight infants: a review. 1231 6

The tocopherol transfer protein (TTP) is a member of the CRAL-TRIO family of lipid binding proteins that facilitates vitamin E transfer between membrane vesicles in vitro. In cultured hepatocytes, TTP enhances the secretion of tocopherol to the media; presumably, tocopherol transfer is at the basis of this biological activity. The mechanism underlying ligand transfer by TTP is presently unknown, and available tools for monitoring this activity suffer from complicated assay procedure and poor sensitivity. We report the characterization of a fluorescent vitamin E analogue, (R)-2,5,7,8-tetramethylchroman-2-[9-(7-nitrobenz[1,2,5]oxadiazol-4-ylamino)nonyl]chroman-6-ol (NBD-TOH), as a sensitive and convenient probe for the ligand binding and transfer activities of TTP. Upon binding to TTP, NBD-TOH fluorescence is blue shifted, and its intensity is greatly enhanced. We used these properties to accurately determine the affinity of NBD-TOH to TTP. The analogue binds to TTP reversibly and with high affinity (K(d) = 8.5 +/- 6 nM). We determined the affinity of NBD-TOH to a TTP protein in which lysine 59 is replaced with a tryptophan. When occurring in humans, this heritable mutation causes the ataxia with vitamin E deficiency (AVED) disorder. We find that the affinity of NBD-TOH to this mutant TTP is greatly diminished (K(d) = 71 +/- 19 nM). NBD-TOH functioned as a sensitive fluorophore in fluorescent resonance energy transfer (FRET) experiments. Using the fluorescent lipids TRITC-DHPE or Marina Blue-DHPE as a donor or an acceptor for NBD-TOH fluorescence, we obtained high-resolution kinetic data for tocopherol movement out of lipid bilayers, a key step in the TTP-facilitated ligand transfer reaction.
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PMID:Utility of a fluorescent vitamin E analogue as a probe for tocopherol transfer protein activity. 1643 Feb 3

alpha-Tocopherol is a member of the vitamin E family that functions as the principal fat-soluble antioxidant in vertebrates. Body-wide distribution of tocopherol is regulated by the hepatic alpha-tocopherol transfer protein (alphaTTP), which stimulates secretion of the vitamin from hepatocytes to circulating lipoproteins. This biological activity of alphaTTP is thought to stem from its ability to facilitate the transfer of vitamin E between membranes, but the mechanism by which the protein exerts this activity remains poorly understood. Using a fluorescence energy transfer methodology, we found that the rate of tocopherol transfer from lipid vesicles to alphaTTP increases with increasing alphaTTP concentration. This concentration dependence indicates that ligand transfer by alphaTTP involves direct protein-membrane interaction. In support of this notion, equilibrium analyses employing filtration, dual polarization interferometry, and tryptophan fluorescence demonstrated the presence of a stable alphaTTP-bilayer complex. The physical association of alphaTTP with membranes is markedly sensitive to the presence of vitamin E in the bilayer. Some naturally occurring mutations in alphaTTP that cause the hereditary disorder ataxia with vitamin E deficiency diminish the effect of tocopherol on the protein-membrane association, suggesting a possible mechanism for the accompanying pathology.
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PMID:Mechanisms of ligand transfer by the hepatic tocopherol transfer protein. 1845 85