Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neutrophils and monocytes are the prime defenders of the body against suppurative bacterial and fungal infections. To accomplish their role in inflammation, they must respond appropriately to chemotactic signals elaborated from complement and bacteria. This response predictably results in the adherence and subsequent directed movement of the phagocytes toward the infected area where they recognize opsonized microbes. Attachment of the microbes to the membrane of the cell leads to their ingestion and subsequent demise, principally by the reduced oxygen by-product H2O2, which is generated by the neutrophils and monocytes during phagocytosis. Optimal killing requires the translocation of granule myeloperoxidase into the phagocytic vacuole containing the bacteria and a suitable halide ion. Degranulation is controlled, in part, by assembled microtubules whereas ingestion requires assembly of submembrane microfilaments. Deficiency states resulting from vitamin E results in diminished membrane-related chemotaxis and ingestion, whereas depletion of cellular GSH results in defective microtubule assembly preventing the normal increase in adherence, chemotaxis, degranulation, and microbicidal activity of the phagocytic cells. Deficiency states resulting in dysfunction of the microtubule system include neutrophil glutathione synthetase deficiency, rodent glutathione peroxidase deficiency, and the Chediak-Higashi syndrome.
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PMID:Role of membrane vitamin E and cytoplasmic glutathione in the regulation of phagocytic functions of neutrophils and monocytes. 39 94

Protein-energy malnutrition in Kivu is associated with a discrete normocytic, normochromic anemia. An attempt to define the physiopathology of this anemia disclosed the following results. As compared with local controls, both iron and total iron binding capacity were low, but with siderophilin saturation and sideroblast counts either normal or elevated; serum and erythrocyte folate was normal, plasma vitamin B12 was normal or elevated, and serum ascorbic acid was normal or elevated. The riboflavin nutritional status was normal. During refeeding, iron and riboflavin deficiencies became apparent. Characteristic findings on admission were the presence of giant erythroblasts and a diminished erythrocyte survival time implicated to an intracorpuscular hemolysis. Two results from the present study could contribute to explanation for the aforementioned abnormalities: low plasma vitamin E levels and, perhaps more importantly, low plasma selenium levels. In conclusion, the anemia of protein-energy malnutrition, as observed in Kivu, is a classifiable nonadaptive anemia that cannot be explained by isolated iron or vitamin deficiencies and whose physiopathology is distinct from that of the anemia of chronic disorders. It is suggested that a selenium deficiency may play an important role in the pathogenesis of this anemia.
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PMID:Protein-energy malnutrition and anemia in Kivu. 41 29

Cardiomyopathy was produced in 38 weanling swine by feeding a semisynthetic diet deficient in selenium and vitamin E for 13 to 59 days. Pigs were killed for morphologic studies of the cardiac lesions at sequential times after development of the deficiency disease. Gross examination disclosed hydropericardium and scattered pale streaks and patches of necrosis in the myocardium, especially the left ventricle. Histopathologically, the lesions were scattered throughout the heart but were most severe in the atria. Ultrastructurally, the damaged fibers had many features of myofibrillar degeneration with hypercontraction bands, myofibrillar lysis, and mitochondrial swelling, disruption, and mineralization. Numerous macrophages appeared to have passed through focal disruptions in the external laminae of the muscle cells and engulfed sarcoplasmic and nuclear debris. Stromal collapse and mild fibrosis persisted as residual lesions in scattered areas of myocardium in pigs with long term deficiency. Although vascular lesions were present in the hearts of selenium and vitamin E deficient pigs, it was concluded that the fiber alterations developed independently of the vascular changes. The pathogenesis of this cardiomyopathy induced by nutritional deficiency is thought to be related to lack of protection by the selenoenzyme, glutathione peroxidase, and the antioxidant, vitamin E, from lipoperoxidative damage.
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PMID:Ultrastructural alterations in nutritional cardiomyopathy of selenium-vitamin E deficient swine. I. Fiber lesions. 88 81

C57BL/6J male mice responded to dietary deficiency of vitamin E with reduction in spermatogenesis. Sex behavior and seminal vesicle weight were unaffected. Supplements of alphabeta-tocopherol (vitamin E) at 0.33 or 72 IU per day maintained spermatogenesis but did not affect seminal vesicles or sex behavior.
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PMID:Vitamin E and sex behavior in mice. 118 70

In this survey of vitamin levels in 93 acute geriatric admissions to hospital, none had a completely normal nutritional profile. Twenty-two patients had over 50% of test abnormal and for all patients the average % of abnormal tests was 29%. The most common abnormalities were albumin, leucocyte vitamin C, vitamin E, carotene and nicotinic acid where over 50% of patients had abnormal results. Transferrin and vitamin A levels were abnormal in over 30% of patients while there was little evidence for riboflavin or thiamine malnutrition. It is postulated that an inadequate dietary intake, due to disease or to physical and mental deterioration was the most likely cause of these multiple nutritional abnormalities.
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PMID:A nutritional survey in the elderly: blood and urine vitamin levels. 121 71

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs).
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PMID:Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans. 137 46

Two children, aged 11 years, who originally had jejunal atresia corrected in the neonatal period, developed massive dilatation of the proximal small intestine. This resulted in circular muscular hypertrophy with lipofuscin deposits giving the typical appearance of "brown bowel." The condition was associated with malnutrition and vitamin E deficiency. Because of relatively short bowel, the condition was treated by limited resection and extensive tapering of the dilated segment, end-to-end reanastomosis, vitamin E supplementation, and intensive nutritional support.
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PMID:Brown bowel syndrome: a late complication of intestinal atresia. 146 88

Measurements of nutritionally relevant biochemical and endocrine variables were made on 60 apparently healthy children (group A) whose parents suffered from leprosy and who had been separated at the age of 4 years and brought up in preventoria. Most of the measurements were also made on a comparison group of healthy children from the same poor socio-economic class (group B). In both groups the serum concentrations of cholesterol and triglycerides were well below those found in Western populations. Almost all the children in both groups were anaemic, but serum iron and ferritin levels were satisfactory. Folate and vitamin B12 levels were measured in group A only and were low in a significant proportion. Deficiency of these water-soluble vitamins may be a cause of the anaemia. Low albumin levels were found in 40% of group A children, compared with 2% in group B. The concentrations of calcium and magnesium were lower and that of phosphate higher in group A than in B. In both groups one-third of the children had low levels of serum zinc. Fifteen per cent of group A children had biochemical evidence of vitamin A deficiency, but none were deficient in vitamin E. Levels of total T3 and total T4 were below the lower limit of normal in a substantial proportion of children in both groups. Concentrations of parathyroid hormone were increased in parallel with the low values for serum calcium. Radiological studies of ossification centres in 57 group A children showed delayed maturation in 11 cases. The relevance of these findings to previous studies of the children of lepers in India is discussed.
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PMID:Nutritional status of children of urban leprosy patients staying at preventoria based on biochemical parameters. 148 18

Food records confirm that there is a high risk of malnutrition at high altitudes because of the usual lack of fresh food. As to the use of pharmacologic properties of micronutrients, only some data on vitamin E are described. Two placebo-controlled studies showed that a prolonged stay at high altitude caused a decrease in physical performance and a deterioration of blood flow, most probably because of increased lipid peroxidation. Supplementation with vitamin E prevented these changes. More research is desirable to obtain valid data on nutritional requirements and to obtain the basis for special recommendations for nutrition at high altitude.
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PMID:Nutrition at high altitude. 154 47

The association between plasma ferritin concentration and vitamin A and E status was studied in 17 children aged 15-72 months with severe oedematous malnutrition. The controls were 10 children of similar age who were apparently well and with no obvious signs of clinical malnutrition. Plasma ferritin concentration in the patients was significantly higher than that in the control children. Conversely, the plasma concentrations of beta-carotene, alpha-tocopherol and retinol in patients were significantly lower than those in plasma of control children. The median (interquartile range) plasma alpha-tocopherol concentration of patients, 6.03 (5.29-9.50) mumol/l, is below the threshold of vitamin E deficiency (11.6 mumol/l). Fifteen of 17 (88%) malnourished patients were found to have plasma tocopherol concentrations below the normal threshold. However, all the patients had a tocopherol: cholesterol ratio greater than 2.22, indicating adequate vitamin E status for the level of cholesterol present in plasma. Twelve of 17 patients (70.5%) had plasma retinol concentration less than 0.70 mumol/l, indicative of marginal vitamin A status, while 3 patients had plasma retinol concentrations less than 0.35 mumol/l, indicating vitamin A deficiency. The median (interquartile range) plasma retinol concentration of patients, 0.51 (0.41-0.93) mumol/l, is significantly less than that of control children, 0.96 (0.74-1.09) mumol/l; p less than 0.01 Mann Whitney U test. Furthermore, anaemia (Hb less than 110 g/l) was widespread in the patients. The results also indicate no significant correlation between elevated ferritin concentration and the concentrations of beta-carotene, retinol and alpha-tocopherol in the patients' plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma ferritin concentration in relation to vitamin A and E status of children with severe oedematous malnutrition. 171 50


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