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 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

Rats of three age groups were fed tocopherol deficient or supplemented diets for 16 weeks or until signs of tocopherol deficiency were apparent. Erythrocyte hemolysis and liver tocopherol content were used as measurements of the tocopherol status of the rats. The following measurements were made on liver microsomal and mitochondrial fractions of all three groups; phospholipid content, lipid peroxidation, fatty acid patterns, pigment fluorescence, ANS fluorescence and the activities of several membrane bound enzymes. Eleven week-old rats displayed signs of vitamin E deficiency after consuming the diet for 7 weeks. Forty-two-week-old rats displayed borderline deficiency signs after 16 weeks of consuming the diet whereas 67-week-old rats displayed no deficiency signs. The need for dietary tocopherol, therefore, appeared to decrease with increasing animal age. Age related alterations in membrane compositional and functional parameters were not modified by either tocopherol deficient or supplemented diets. Tocopherol does not appear to stabilize microsomal membrane composition or function although mitochondrial membranes appear to be labilized by the dietary manipulation of the vitamin.
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PMID:Effect of dietary alpha tocopherol on liver microsomes and mitochondria of aging rats. 93 28

The vitamin E deficiency was studied for its effect on the activity of enzymes participating in metabolism of xenobiotics. Experiments with 54 rats have demonstrated that the maintenance of animals on the vitamin-E-deficient diet within 13-14 weeks decreases the activity of microsomal monooxygenases (demethylase and hydroxylase), NADH- and NADPH-reductases, aryl- and aliesterases in the liver and lungs, which is a result of disturbance of hydrophobic and polar interactions in microsomal membranes. Vitamin E deficiency makes the extent of solubilization of these enzymes higher under the influence of deoxycholate and trypsin and intensifies inactivation of these enzymes under the effect of urea. In the lungs and in the liver of the vitamin E deficient rats the content of reduced glutathione decreases as well as the activity of glutathione reductase, glutathione-S-transferase, aldehyde dehydrogenase, while the activity of gamma-glutamyltransferase increases; glutathione disulphide is accumulated.
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PMID:[The effect of vitamin E deficiency on enzyme activity and the status of the membrane fraction of rat liver microsomes]. 258 40

Lipid peroxidation of microsomal membranes isolated from rat liver, and Morris hepatomas 9618A (slow-growing) and 3924A (fast-growing) was induced by superoxide radicals generated by the action of xanthine oxidase on xanthine. The peroxidation, measured as malondialdehyde and lipid hydroperoxide formation, was optimized with regard to iron concentration and chelation of iron by ADP. In such conditions hepatoma microsomes catalyze lower rates of lipid peroxidation than the normal counterpart. However, while microsomes from hepatoma 3924A show a marked decrease in both the malondialdehyde and hydroperoxide production rates, microsomes from hepatoma 9618A differ moderately from the control, mainly in the long-term production of hydroperoxides. It is also reported here that the 9618A microsomes partially lack cytochrome P-450 (about 40% deficiency), but they have a fatty acid composition similar to that of control. No differences were found in the content of vitamin E between normal and hepatoma 3924A microsomes. Moreover, induction of vitamin E deficiency in hepatoma 3924A microsomes does not influence the rate of either malondialdehyde or lipid hydroperoxide production. On the basis of these results and previous data on the lipid composition of hepatoma 3924A microsomes it is proposed that the high resistance to superoxide-dependent lipid peroxidation of hepatoma 3924A microsomes is related to the low substrate availability rather than the content of membrane antioxidants; and a limitation only in the propagation phase characterizes the hepatoma 9618A microsomal lipid peroxidation and would be due to the partial deficiency of the endogenous propagating agent, cytochrome P-450.
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PMID:Superoxide-dependent lipid peroxidation and vitamin E content of microsomes from hepatomas with different growth rates. 298 56

Vitamin E, a dietary antioxidant, is known to inhibit peroxidation of membrane lipids and to protect the lungs of vitamin E-deficient animals and to a lesser extent vitamin E-sufficient animals from oxidant injury. Since the protective interaction between vitamin E and biological membranes may be related to alterations in composition and physical state of membrane lipids, we evaluated the effect of vitamin E deficiency on lung microsomal lipids and membrane fluidity. Both intact microsomes and lipid vesicles prepared from the total lipid extracts of these microsomes were used. The percentage incorporation of vitamin E and cholesterol, membrane fluidity, and lipid peroxidation were measured in microsomes as well as their lipid vesicles. Fluidity was measured by monitoring changes in fluorescence anisotropy for 1,6-diphenyl-1,3,5-hexatriene (DPH). Lipid peroxidation was measured by thiobarbituric acid reaction. There were significant increases in the phospholipid (p less than 0.01), the total cholesterol (p less than 0.05), and the total saturated fatty acids (p less than 0.05) and decreases in total polyunsaturated fatty acid (p less than 0.01) content of vitamin E-deficient microsomes. There were no detectable peroxidative products in freshly isolated microsomes from either vitamin E-sufficient or -deficient lungs. However, lipids from vitamin E-deficient microsomal membranes were more susceptible to free radical initiated peroxidation than lipids from vitamin E-sufficient microsomes. Fluidity in vitamin E-deficient microsomes or in their lipid vesicles was significantly (p less than 0.05) decreased compared to the respective controls. In vitamin E-deficient microsomes or their lipid vesicles, the incorporation rate of vitamin E was two- to three-fold greater than in vesicles of vitamin E-sufficient microsomes or their lipid vesicles. However, the percentage incorporation of cholesterol was identical in both vitamin E-deficient and vitamin E-sufficient microsomes or in their respective lipid vesicles. As a result of vitamin E incorporation, fluidity was significantly decreased (p less than 0.05) in vitamin E-sufficient vesicles and was further decreased (p less than 0.001) in vitamin E-deficient vesicles. Incorporation of cholesterol also decreased fluidity in both vitamin E-deficient and vitamin E-sufficient vesicles but to the same extent (p less than 0.001). Lipid peroxide formation was two-fold greater in the vitamin E-deficient than in the vitamin E-sufficient vesicles.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vitamin E, membrane order, and antioxidant behavior in lung microsomes and reconstituted lipid vesicles. 318 15

Lipid peroxidation of rat liver microsomal fractions was monitored by its low-level chemiluminescence in preparations from controls and vitamin-E-deficient animals. Measurements were made (a) of the duration of the lag phase tau0 after initiation with NADPH/iron-ADP and (b) of the slope of the chemiluminescence increase. In microsomes with normal vitamin E (alpha-tocopherol) level the lag phase tau0 was substantially increased by ascorbate; in contrast, even an enhanced peroxidation was observed with ascorbate in vitamin-E-deficient microsomes. Therefore, the ascorbate-mediated protection of microsomal membranes against lipid peroxidation is dependent on vitamin E in the membrane. In vitamin E deficiency the pro-oxidant effect of ascorbate was abolished when glutathione (GSH) was present. Likewise, GSH does not prolong the lag phase tau0 in vitamin E deficiency. However, GSH (but not cysteine) exerts an antioxidant effect both in controls and in vitamin E deficiency by decreasing the slope of the chemiluminescence increase during lipid peroxidation. The involvement of GSH in an enzyme-dependent mechanism is suggested.
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PMID:The protection by ascorbate and glutathione against microsomal lipid peroxidation is dependent on vitamin E. 338 50

For 90 days male August rats were kept on 5 diets: (I) balanced semisynthetic, (II) with amino acid unbalance, (III) with excess polyunsaturated fatty acids (PUFA), (IV) with vitamin E deficiency, and (V) polyunbalanced (amino acid unbalance, excess PUFA, vitamin E deficiency). In liver microsomes, the authors studied the kinetics of malonic dialdehyde accumulation in the course of NADPH-dependent lipid peroxidation (LP) and microviscosity of the lipid phase of microsomal membranes according to eximerization of the pyrene fluorescent hydrophobic probe. The microsomes of the animals fed diets I, III and IV showed on the average a 50 to 55% increase in the rate of MDA formation, whereas those of rats on diet V a 78% increase as compared with appropriate characteristics in the animals fed diet I. A good correlation was established between the decrease in the pyrene eximerization rate and accumulation of lipid peroxides: r = 0.09 (P less than 0.05). The possibility of affecting LP in the membranes by the goal oriented modification of the diet is discussed. The participation of proteins, lipids and tocopherol in the maintenance of the membrane structure is described.
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PMID:[Effects of different types of nutritional imbalance on lipid peroxidation and viscosity of membrane lipids]. 396 68

The effect of the vitamin E status of membranes on the balance between pro- and antioxidant activity of ascorbic acid was studied in microsomes from rat heart, kidney and liver. Lipid peroxidation was initiated by 5 microM ferrous ions, in combination with amounts of ascorbic acid ranging from 0-4 mM. Lipid peroxidation was assessed after 1 h of incubation as production of thiobarbituric acid reactive material. It was found that the vitamin E status of the microsomal membranes had little effect on the balance between pro- and antioxidant activity of vitamin C. The sensitivity of the membranes to ferrous ions/ascorbic acid-induced lipid peroxidation, however, was highly dependent on the vitamin E content of the membranes. Vitamin E depletion, in combination with different ascorbic acid concentrations, showed that vitamin E deficiency is not an incontestable model system for enhanced sensitivity to lipid peroxidation in all organs.
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PMID:Effect of vitamin E on the balance between pro- and antioxidant activity of ascorbic acid in microsomes from rat heart, kidney and liver. 400 46


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