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Query: UMLS:C0026850 (muscular dystrophy)
 5,870 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Comparison of the skeletal muscles from vitamin E-deficient and control rabbits showed that the muscles from the deficient animals had lower contents of protein and glycogen but more water and lipid. Increases of individual lipids per unit weight of muscle from deficient animals compared with those from control animals were 2.2-fold for gangliosides, 2.18-fold for cholesterol, 1.74-fold for sulfatides, and 1.45-fold for neutral glycosylceramides. Total phospholipids did not change; this was the result of an increase in sphingomyelin (1.47-fold) and a decrease of phosphatidylcholine to 83% of the control, while the other fractions remained unchanged. When the measurements were referred to total muscle, the contents of cholesterol, gangliosides, sulfatides, neutral glycosylceramides, and sphingomyelin in muscle from vitamin E-deficient rabbits were also above those of the control rabbits, and only the phosphatidylcholine content was decreased. It was not possible to determine whether the alteration of lipid content preceded or followed the onset of signs of muscular dystrophy.
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PMID:Changes of gangliosides and other lipids in skeletal muscle from rabbits with experimental dystrophy. 435 42

Vitamin E refers to a family of fat-soluble phenolic compounds called tocopherols, which have been established as essential nutrients in vertebrates. In animals the deficiency state has resulted in diminished reproductive capabilities, muscular dystrophy, exudative diathesis, megaloblastosis, gastrointestinal and pulmonary degeneration, and nephrosis. In humans with low vitamin E levels a subclinical diminished erythrocyte life-span has been demonstrated by hydrogen peroxide hemolysis test. This effect may have clinical significance among premature infants. The metabolic function of vitamin E appears to be as a scavenger of lipid peroxides and free oxygen radicals which enter into chain reactions to cause breakdown of lipids. Normal levels of the vitamin serve to prevent this cellular oxidative breakdown. Laboratory measurement of vitamin E is chromatographic, with HPLC presently used in both research and clinical applications. The association between vitamin E levels and hemolytic anemia in humans is currently under investigation.
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PMID:Vitamin E and autoxidation. 634 59

Outbreaks of alopecia with unusually high morbidity occurred among calves reared on milk substitutes on two unrelated farms in Suffolk. On one farm alopecia occurred for three consecutive years; during the winter of 1981-82 there were also clinical signs of muscular dystrophy among the same calves. On the second farm calves with alopecia also showed signs of muscular dystrophy. The apparent relationship between alopecia and milk substitute feeding is discussed together with the possible involvement of vitamin E.
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PMID:Alopecia in calves associated with milk substitute feeding. 686 7

Muscular dystrophy and cardiomyopathy were produced in weanling rats by feeding a vitamin E-deficient diet for 12 mth. Deficient and control rats were killed, and skeletal muscle and myocardium were used for subcellular studies and biochemical assay of selected lysosomal enzymes. Ultrastructurally, the skeletal muscle showed various degrees of pathological changes. In the severely damaged muscle fibres, prominent increase of secondary lysosomes, autophagic vacuoles, residual bodies, disappearance of myofilaments, rupture of sarcolemma and shrinkage of muscle fibres were noted. The damaged muscle fibres finally became dense residual bodies and dispersed in the interstitial spaces, where the macrophages and fibroblasts were found. In the myocardium, some muscle fibres were intact with mild fatty infiltration and marked proliferation of mitochondria. However, in the severely damaged myocardial fibres, the whole fibre was always filled with amorphous dense bodies, and the sarcolemma was ruptured. This resulted in dispersion of many cellular organelles in the surrounding interstitial space. A significant increase of cathepsin and beta-glucuronidase activity in the cytosol of both organs suggests that lysosomal enzymes may play a major role in the destruction of muscle and cardiac fibres in the long-term vitamin E-deficient animals.
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PMID:Ultrastructural and lysosomal enzyme studies of skeletal muscle and myocardium in rats with long-term vitamin E deficiency. 715 34

It is shown that E-hypovitaminosis-induced muscular dystrophy in rabbits is accompanied by a sharp decrease in the body mass, an increase in the urine creatine-index, a decrease in the vitamin E and ubiquinone contents in the liver and skeletal muscle tissues. In the myocardium mitochondria a decrease in the vitamin E content and an increase in the ubiquinone content are observed. The activity of NADH-cytochrome c-, NADH-ubiquinone- and succinate-ubiquinone-reductase also varies in mitochondria of the studied tissues. In myocardium organellas a direct dependence is found between the content of ubiquinone, NADH- and succinate-ubiquinone-reductase activity and an inverse one-between its content and the activity of the NADH-cytochrome c-reductase system. It is established that p-oxybenzoic acid as well as vitamin E prevents development of muscular dystrophy and causes changes analogous in direction in the activity of the ubiquinone-dependent enzymic systems of mitochondria. Ubiquinone-9 is less efficient in preventing the development of muscular dystrophy.
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PMID:[Efficiency of ubiquinone and p-oxybenzoic acid in prevention of E-hypovitaminosis-induced development of muscular dystrophy]. 729 23

Vitamin E levels were measured in the plasma of infants and children with various neuromuscular disorders. Seven of 8 infants with Werdnig-Hoffmann disease (WHD) had a significantly lower plasma vitamin E level (p less than 0.01) than age-matched normal controls, children with congenital myopathies, or children with muscular dystrophy. Vitamin E deficiency in WHD is not caused by malabsorption. A therapeutic trial of vitamin E in 3 patients with WHD did not change the natural course of the disease. Vitamin E deficiency may play a role in the pathogenesis of WHD.
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PMID:Vitamin E deficiency in Werdnig-Hoffmann disease. 729 34

Activity of vitamin E and its derivatives--alpha-tocopheryl quinone, its short chain analogue and alpha-tocopheryl acetate also containing short chain molecule were studied during chicken experimental muscular dystrophy. alpha-Tocopheryl quinone containing short chain molecule proved to be the most active substance; similarly to vitamin E the preparation increased the erythrocyte resistance to osmotic haemolysis, distinctly increased the content of ubiquinone and decreased concentration of ubichromenol in the chicken liver tissue as compared with E-deficient animals. At the same time, the content of ubiquinone was unaltered in skeletal muscles. The data obtained suggest that vitamin E could be effectively substituted by its derivatives for prevention an treatment of muscular dystrophy.
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PMID:[Effectiveness of different alpha-tocopherol derivatives in preventing experimental muscular dystrophy in chickens]. 733 51

Till date, many workers have demonstrated the nutritive value of dietary lipids and the qualitative and quantitative requirements for essential fatty acid (EFA) in many cultivable fish. From the data accrued, a categorization can be made for the EFA requirement as follows: Type I (require n-6 fatty acids), Type II (require both n-6 and n-3 fatty acids) and Type III (require n-3 fatty acids). Common carp Cyprinus carpio and grass carp Ctenopharyngodon idella are codified as Type II fish based on their EFA needs. The requirement of both fish for dietary n-6 and n-3 fatty acids is found to be 1% and 0.5-1%, respectively. Our recent experiment clearly indicated that grass carp fed diet without EFA show deficiency symptoms like vertebral column curvature (VCC), indicating lordosis. The manifestation is similar to SEKOKE DISEASE which is characterised by apparent muscular dystrophy. However, grass carp fed an EFA-deficient diet did not exhibit the apparent muscular dystrophy. Recently, we have also investigated the interaction between EFA and vitamin E (VE), and the metabolism of linoleic acid (LA) using the isotope technique. These results are to be reviewed.
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PMID:Essential fatty acid requirements in carp. 876 70

Because of the very low concentrations of selenium in the dry matter of grass, grass silage, hay and maize silage Slovenian dairy herds need to be supplemented with selenium. Selenium in the form of mineral and feed mixtures maintained adequate mean (sd) blood serum selenium concentrations of 43.9 (27.6) to 65.3 (18.5) micrograms/litre in lactating cows, but in late lactation and in the dry period when only mineral mixtures were used, about 60 per cent of the cows had marginal serum selenium concentrations, mainly because of the low intake of the mineral supplement. In 18 herds which were either unsupplemented or irregularly supplemented with selenium, the mean (sd) concentrations in blood serum were 13.7 (5.5) micrograms/litre and 17.4 (9.2) micrograms/litre, respectively, for selenium and 2.98 (2.72) mg/litre and 1.62 (1.73) mg/litre for vitamin E, indicating that under extensive farming conditions in Slovenia the lack of both micronutrients may be responsible for nutritional muscular dystrophy in calves. Among 37 clinical cases, cardiorespiratory signs predominated in 25 of the calves and skeletal myopathy was dominant in 12. A very low mean serum selenium concentration [9.7 (7.2) micrograms/litre] and typically high activities of aspartate aminotransferase (AST) [1125 (373) U/litre] and creatine kinase (CK) [9169 (3681) U/litre) were observed for the myocardial form of the disease, and 2797 (550) U/litre and 22,650 (13,500) U/litre were observed for the skeletal form of the disease. A highly significant (P < 0.0001) difference in the selenium concentration of liver dry matter between the regularly supplemented [402 (207) micrograms/kg] and irregularly supplemented [173 (69) micrograms/kg] herds was observed. If a minimum value of 300 micrograms/kg of liver dry matter is accepted as the criterion for the determination of adequate selenium status, 93 per cent of the samples from the irregularly supplemented herds were selenium deficient. A similar proportion was estimated to be selenium deficient when the criterion was taken to be 30 micrograms selenium/litre of blood serum.
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PMID:Assessment of selenium and vitamin E deficiencies in dairy herds and clinical disease in calves. 891 12

The Food and Nutrition Board of the Institute of Medicine recently published a comprehensive evaluation of antioxidants in human diets that includes dietary reference intakes for vitamin E. The new dietary reference intake is 15 mg (35 mol)/d for adults, which is 50% greater than the generous allowance in the 10th edition of Recommended Dietary Allowances published in 1989. Much of the data interpreted in these publications came from studies sponsored by the Committee of Nutritional Studies at Elgin State Hospital (Elgin, IL) of an earlier Food and Nutrition BOARD: The 50% increase in the recommended dietary allowances for vitamin E is not supported by any new data. It is possible that the publication of the Institute of Medicine did not take into consideration the effects of the oxidized lipids in the diets used to promote the development of vitamin E deficiency. If lipids, oxidized to remove tocopherols, had not been a part of the experimental diets, the minimum requirement for vitamin E would have been too small for possible evaluation. Studies on the different effects of saturated and oxidized lipids in the production of encephalomalacia in chicks and muscular dystrophy in rats are reviewed. The tolerable upper intake level of vitamin E supplementation is reported to be 1000 mg/d. It is possible that the universal consumption of aspirin may not have been taken into consideration when this level was determined. Vitamin E plus aspirin may increase the tendency to hemorrhage, which makes a lower upper intake level worth consideration.
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PMID:Critique of the requirement for vitamin E. 1191 70


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