Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Literature on the various manifestations of the selenium deficiency in humans and animals is presented. Mechanisms of the biological effects of selenium brought about by glutathione peroxidase are considered. Biogeochemical anomalies, parenteral nutrition, malabsorption syndromes as conditions for the development of hyposelenosis are characterized as well as their manifestations (white-muscular disease, myopathies, cardiomyopathies, Keshan disease, Kashin-Beck disease). Selenium deficiency facilitates the development of the ischemic heart disease, myocardium infarction, certain types of malignancy and so on. The attention is drawn to the link of the selenium deficiency with imbalance of other trace elements.
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PMID:[Hyposelenoses]. 212 81

Selenium is an essential trace element in humans and animals. Its only established function in humans is the antioxidant activity of glutathione peroxidase, a selenoenzyme. Severe prolonged deficiency may cause a fatal cardiomyopathy. Iatrogenic causes of selenium deficiency include parenteral and enteral nutrition. Low plasma selenium is also found in malabsorption, cystic fibrosis, rheumatoid arthritis, neoplasia, and other varied clinical disorders. Death has resulted from a single massive ingestion of selenium, while chronic excessive intake causes skin, nail, and hair pathology. Extreme geographical variation in population blood and urine selenium levels and a marked age-specific variation in population reference intervals are important factors in understanding selenium nutrition. Nutritional requirements, biological availability, and metabolism are discussed in relation to geographical, age, and method variability. Sampling, processing procedures, and methods for selenium quantitation are reviewed. Selenium content in different biological matrices and reference values for pediatric, adult, and obstetric populations are provided.
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PMID:Selenium: clinical significance and analytical concepts. 269 Aug 56

Selenium (Se) is a metalloid with chemical properties closed to those of sulfur, but they can not substitute for one another in vivo. Se body content reflected soil Se content (13 to 20 mg in North Americans, 3 to 6 in New Zealand residents). The daily intake recommended is 50 to 200 micrograms. In the diet Se occurs in mineral or organic forms, the bioavailability of these latter is better. Se as selenocysteine is incorporated in specific proteins such as glutathione peroxidase (GSH-Px). Se is metabolized in H2Se by reductive pathways. H2Se is methylated and methylated compounds are excreted in the urines. The Se urinary excretion represents the principal known process of Se regulation. Se bound to GSH-Px participates to free radical destruction and cellular membrane protection. Its role is complementary of vitamin E effect. Se also seems indispensable to appropriate immune response. It can chelate various metals allowing their detoxication. Se metabolism can be studied by Se assay in serum, whole blood, urine (reference values must be performed for each studied population) and by GSH-Px activity determination in erythrocytes or platelets. Vitamin E assay completes estimation of the antioxidative status of organism. Few Se intoxications have been recognized but Se deficiencies often happen. They can lead to a cardiomyopathy (Keshan disease), increase the risk of cardiovascular diseases or cancer. Se deficiencies are found in chronic renal failure, malnutrition malabsorption, long term parenteral nutrition. At the present time it is not known how Se deficiency interfers with chronic infections which often go with these diseases. A better knowledge of Se requirements and Se role could allow an appropriate supplementation in various diseases.
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PMID:[Selenium: physiologic role and value in human pathology]. 305 85

It has been reported that lipid peroxidation increases in patients with antioxidant deficiencies, such as vitamin E and glutathione peroxidase. The relationships between serum lipid peroxide and vitamin E on the one hand and glutathione peroxidase on the other were examined in 22 patients with chronic pancreatitis, often accompanied by malabsorption of fats and fat-soluble vitamins due to the impaired exocrine pancreatic function. Both serum vitamin E concentrations and glutathione peroxidase activities were depressed, especially in patients with chronic calcifying pancreatitis. On the other hand, serum lipid peroxide levels were elevated. A significant negative correlation was found between the serum lipid peroxide levels and vitamin E concentration. These findings suggest than an elevation of the serum lipid peroxide level may be due to the lack of an antioxidative defense mechanism, such as vitamin E, against lipid peroxide.
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PMID:Serum vitamin E, lipid peroxide and glutathione peroxidase in patients with chronic pancreatitis. 721 10

Cystic fibrosis patients are at risk for nutrient deficiencies from malabsorption related to exocrine pancreatic insufficiency. This research examined the copper homeostasis of children with cystic fibrosis. Our objective was to measure cytochrome oxidase and copper-zinc superoxide dismutase activities in mononuclear cells, neutrophils, and erythrocytes of adolescents with cystic fibrosis, as well as plasma copper and ceruloplasmin. Thirteen adolescents with pancreatic insufficiency caused by cystic fibrosis were compared with 10 age- and sex-matched control subjects. Serum copper concentrations and ceruloplasmin measurements were not significantly different between the two groups. Cytochrome oxidase activity was significantly lower in the mononuclear cells and copper-zinc superoxide dismutase activity was significantly lower in the neutrophils and erythrocytes of the cystic fibrosis group. Other measures of trace element status such as hemoglobin concentration, serum ferritin, serum zinc, glutathione peroxidase activity, and manganese superoxide dismutase activity were not different between the two groups. Reductions in the activity of two copper-dependent enzymes suggest abnormal copper homeostasis in this population.
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PMID:Reduced copper enzyme activities in blood cells of children with cystic fibrosis. 766 Nov 26

Cystic fibrosis often combines an infectious pathology with a syndrome of malabsorption, both potentially capable of favoring the deleterious effects of reactive oxygen species. This study was a simultaneous evaluation of the main antioxidant systems dependent on micronutrients and of lipid peroxidation products in 27 children with cystic fibrosis and 17 healthy children. Plasma of cystic fibrosis patients showed very low concentrations of beta-carotene (0.30 +/- 0.2 vs 1.63 +/- 0.5 mumol/g cholesterol, P < 0.0001) and a lower activity of selenium-dependent glutathione peroxidase (263.6 +/- 42 vs 296.9 +/- 57 U/L, P = 0.028). In parallel, the higher plasma concentrations of organic hydroperoxides (171.5 +/- 54.4 vs 122.6 +/- 23.3 mumol/L, P = 0.001) and of thiobarbituric acid reactants (2.9 +/- 0.6 vs 2.4 +/- 0.3 mumol/L, P = 0.004) reflected oxidative stress in this pathology. In addition, in these patients the major substrates of lipoperoxidation were significantly lower, whether they be linoleic acid (2.26 +/- 0.8 vs 3.60 +/- 0.9 mmol/L, P < 0.0001) or arachidonic acid (0.55 +/- 0.2 vs 0.74 +/- 0.2 mmol/L, P = 0.006). These results suggested that nutritional deficiencies resulting from malabsorption could considerably amplify disorders related to toxicity of reactive oxygen species. These nutritional deficits could also be aggravated by the destruction of antioxidant compounds by the inflammatory process.
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PMID:Altered antioxidant status and increased lipid peroxidation in children with cystic fibrosis. 860 62

In cystic fibrosis (CF) patients the antioxidative-oxidative balance is chronically disturbed. Free radicals were generated by bronchial-pulmonal infection and additional exist a deficiency of antioxidative substances by enteral malabsorption especially vitamin E and selenium. Because selenium is an essential content of glutathione peroxidase, which is acting in cytosol and cell membranes, for the present we tested a selenium therapy (peroral sodium selenite 155 micrograms (Se/m2 BSA/d i. e. 4 micrograms Se/kg/d; 4 fold of recommended supply) in 32 CF patients. After three months of this therapy we have seen positive metabolic (normalized content of plasma-selenium, -glutathione peroxidase), endocrine (enhanced efficacy of thyroid hormones, mild increased IgF-I reduced LDL-chol) and clinical consequences (enhanced left ventricular cardiac output), but in three patients side effects (anorexia, nausea, mild hair loss) were observed. Longtime sodium selenite therapy only with 60 micrograms Se/m2 BSA/d over 1 year, stabilized the favourable influences without side effects. For CF patients therefore we recommend a sodium selenite substitution therapy, the best in combination with vitamin E.
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PMID:[The value of selenotherapy in patients with mucoviscidosis]. 771 84

Oxygen free radicals have been implicated as mediators of tissue injury in a variety of diseases. We investigated the role of oxidative injury and oxygen free radical scavengers in liver cell injury associated with obstructive jaundice in Wistar rats. Bile duct ligation for 4 or 7 days led to a decrease in both vitamin E and A in the plasma and liver of male Wistar rats, indicating the malabsorption of lipid-soluble vitamins. Serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase activities were increased in the bile-duct-ligated rats. Furthermore, marked increases in lipid peroxide and oxidized glutathione levels indicated cholestatic liver injury. The antioxidant defense system was impaired, as shown by decreases in reduced glutathione and in the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase. Moreover, these high lipid peroxide levels and low levels of antioxidants correlated with the severity of jaundice. After releasing the bile duct ligation, levels of bilirubin, lipid peroxide and oxidized glutathione declined, while the levels of vitamin E and A, reduced glutathione, and the activities of GSH-Px increased, indicating an improvement in liver function. These findings suggest that lipid peroxidation is associated with the pathogenesis of liver damage in animals with bile duct ligation. Meanwhile, free oxygen radical scavengers are reduced in the bile-duct-ligated rats, thereby increasing the susceptibility of the liver to injury by oxygen-derived free radicals.
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PMID:Biochemical events associated with ligation of the common bile duct in Wistar rats. 903 77

Trace elements constitute important prosthetic groups in a number of antioxidant enzymes which neutralize free radicals generated during inflammatory conditions such as colitis. However, the status of trace elements in colitis remains to be found. In the present study the concentrations of zinc, copper, manganese and selenium in the colon, liver and serum of rats with acetic acid (HAc)- or trinitrobenzenesulfonic acid (TNBS)-induced colitis were measured using atomic absorption spectrophotometer. Myeloperoxidase and glutathione peroxidase activities were measured spectrophotometrically. Our results show that the selenium concentration was significantly decreased by 33 and 37.5% in the colon and 69 and 78% in liver by HAc and TNBS treatment, respectively. Similarly the zinc concentration in the colon was decreased by 21 and 28% by HAc- and TNBS-induced colitis as compared to the controls, but manganese and copper, remained unaltered. The serum concentrations of copper, zinc and selenium also remained unaltered during colitis. The weight of HAc-treated rats did not decrease while there was a significant weight loss in the TNBS-treated rats. Myeloperoxidase activity was increased, whereas glutathione peroxidase activity was significantly decreased in the colon inflamed by HAc or TNBS as compared to the controls. These findings suggest that colitis induces a reduction in the tissue levels of trace elements which is independent of the way colitis is induced. Our findings of a reduction in Se and glutathione peroxidase activity together suggest that the reduction in the trace element concentrations is not due to dietary factors or malabsorption. The decrease may severely affect the antioxidant potential of the colon and therefore is a putative factor for the progression of disease.
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PMID:Colitis-induced changes in the level of trace elements in rat colon and other tissues. 981 22

The aim of the present study was to evaluate the influence of severe protein-energy malnutrition on the antioxidant defense system in the small and large intestine in rats at weaning. Chronic diarrhea and the subsequent malnutrition were induced by oral intake of a lactose-enriched diet. Twenty rats were weaned at 21 days of age, and the control group was fed a semipurified synthetic diet for two weeks. The malnourished group was fed the same diet but carbohydrates were replaced by lactose, and they developed diarrhea one day after. Rats were killed, and macroscopic and histological features were analyzed, DNA content was measured, and alkaline phosphatase, myeloperoxidase, and gamma-glutamyltranspeptidase activities were determined to assess the degree of intestinal injury. Glutathione levels as well as the activities of intestinal glutathione transferase, glutathione reductase, total glutathione peroxidase, selenium-dependent glutathione peroxidase, superoxide dismutase, and catalase were measured to study the antioxidant defense system. Malnourished rats showed loss of body weight and an increase in length and weight in jejunum and ileum, while no significant changes were observed in colon. Epithelial cells showed fewer and shorter microvilli, larger mitochondria with low inner density and loss of cristae, dilated endoplasmic reticulum, and Golgi apparatus. The protein-to-DNA ratio was higher in the jejunum, ileum, and colon of malnourished rats. Glutathione levels decreased 40% in jejunum and 50% in colon of malnourished rats. A 40-50% decrease in the activity of all the enzymes of the antioxidant defense system was observed in the jejunum and ileum of malnourished rats, while only catalase and glutathione transferase activities decreased 50% in colon. These results suggest that early chronic diarrhea and severe protein-energy malnutrition impair the antioxidant defense system in both the small and large intestine, which may have a role in the pathogenesis and maintenance of the vicious circle of malabsorption-diarrhea-malnutrition in infancy.
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PMID:Chronic diarrhea impairs intestinal antioxidant defense system in rats at weaning. 1111 81


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