Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.
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PMID:Comparative effects of selenium and vitamin E in lead-poisoned rats. 84 75

In a 26-year-old patient there have been benign enlargements of the lymphatic nodes and a splenomegaly since the end of the adolescence. In the 21st year of age the diagnosis of a Tangier disease was made. Allogenic HDL-rich serum fraction (COHN IV/1-fraction, prepared according to the modified method 6) infused under therapeutic aspect led to a prolonged increase of the serum total cholesterol and of the thrombocytes. The results pled for an activation of the reverse cholesterol transport. Excessively high malonic dialdehyde concentrations in the serum were relating to a "free radical"-associated metabolic defect, which was caused by the hypocholesterolaemia, the reduced transport capacity of vitamin E in the plasma and the nutrition poor in selenium and cholesterol, respectively. Under a nutritive antioxidant supplementation with sodium selenite and D-alpha-tocopherol a slight increase of the total cholesterol, of the thrombocytes as well as a normalization of the MDA values could be reached. The chronic oxidative stress appeared in the patient in a distinct lipofuscinosis of the skin and formations of naevus-cell naevi as an expression of massive denaturations of protein-lipids. In the Tangier disease we must reckon with an increased mutagenic effect of free radicals with an additional DNS repair capacity as well as an increased sensitivity to radical-generating cancerogenic xenobiotics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tangier disease--a "free radical"-associated disease. Results of HDL and anti-oxidant therapy with selenium and D-alpha tocopherol]. 166 43

The hepatoprotective action of the Romanian preparation Orgasel containing selenium (Se) 5.01 mg/100 g autolysated yeast powder, was tested on adult Wistar rats poisoned with carbon tetrachloride (CCl4). The hepatotoxic agent (a 20% CCl4 solution in oil) was administered i.p. in a single dose of 0.3 ml CCl4 solution/100 g body weight, and the preparation tested (autolysate of seleniated yeast) was administered by gavage in 4 doses (of 100 mg Se powder/100 g animal each) along 2 days. After 48 hrs the animals were sacrificed, then their blood and liver were collected. The treatment with Orgasel significantly reduced the organs, morphological changes (fat liver degeneration, splenomegaly, testicle degeneration) induced by CCl4 poisoning in the rat, an effect found also at the biological parameters levels studied in plasma and liver. In the plasma, the high lipid peroxide concentrations, the increased activity of alkaline phosphatases, and the reduced antioxidative activity generated by CCl4 have been statistically significant brought to the normal range after Orgasel administration. At the liver this treatment significantly decreased the lipid peroxides production, the total lipids and cholesterol concentrations, and statistically significant increased the enzymes activity (alkaline phosphatases, GPT). The results obtained after Orgasel administration proved that this preparation has a global beneficial action upon the organism in the poisoned rat, as well as a strong antioxidative effect, confirming once again the essential role of Se in maintaining cells' integrity.
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PMID:The influence of "selenium organicum" upon the hepatic function of carbon tetrachloride poisoned rats. 853 46

LP-BM5 Murine leukemia virus (MuLV) infection of C57BL/6 mice develop a disease that has many features in common with human acquired immunodeficiency syndrome (AIDS), in particular abnormal lymphoproliferation and severe immunodeficiency. Thus, this MAIDS model may be useful for evaluation of potent antirival agents in vivo. Deficiency in antioxidant micronutrients such as selenium, zinc, and glutathione have been observed in AIDs and AIDS-related complex (ARC) patients. In the present study, the MAIDS model was used to evaluate immunological and oxidative effect of Se as sodium selenite. Results indicated that Se treatment 0.1 mg/kg/d (p.o.) inhibited splenomegaly and sera IgG elevation effectively. In addition to abnormal immunity, oxidative imbalance possibly existed in MAIDS model, as lipid peroxide increased significantly in spleen and whole blood glutathione peroxidase (GSH-Px) activity decreased markedly. Se supplementation had good protective effect.
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PMID:Effect of selenium supplementation on mice infected with LP-BM5 MuLV, a murine AIDS model. 952 61

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.
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PMID:Two fatal cases of selenium toxicity. 1689 Oct 71

Systemic lupus erythematosus (SLE) is a debilitating multi-factorial immunological disorder characterized by increased inflammation and development of anti-nuclear autoantibodies. Selenium (Se) is an essential trace element with beneficial anti-cancer and anti-inflammatory immunological functions. In our previous proteomics study, analysis of Se-responsive markers in the circulation of Se-supplemented healthy men showed a significant increase in complement proteins. Additionally, Se supplementation prolonged the life span of lupus prone NZB/NZW-F1 mice. To better understand the protective immunological role of Se in SLE pathogenesis, we have investigated the impact of Se on B cells and macrophages using in vitro Se supplementation assays and the B6.Sle1b mouse model of lupus with an oral Se or placebo supplementation regimen. Analysis of Se-treated B6.Sle1b mice showed reduced splenomegaly and splenic cellularity compared to untreated B6. Sle1b mice. A significant reduction in total B cells and notably germinal center (GC) B cell numbers was observed. However, other cell types including T cells, Tregs, DCs and pDCs were unaffected. Consistent with reduced GC B cells there was a significant reduction in autoantibodies to dsDNA and SmRNP of the IgG2b and IgG2c subclass upon Se supplementation. We found that increased Se availability leads to impaired differentiation and maturation of macrophages from mouse bone marrow derived progenitors in vitro. Additionally, Se treatment during in vitro activation of B cells with anti-CD40L and LPS inhibited optimal B cell activation. Overall our data indicate that Se supplementation inhibits activation, differentiation and maturation of B cells and macrophages. Its specific inhibitory effect on B cell activation and GC B cell differentiation could be explored as a potential therapeutic supplement for SLE patients.
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PMID:Selenium supplementation suppresses immunological and serological features of lupus in B6.Sle1b mice. 3100 65