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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The separate administration of mercuric chloride (HgCl2) and sodium selenate (Na2SeO4) to male rats in drinking water or a combined administration of both (50 ppm Hg, 15 ppm Se) caused different signs of toxicity over a 22 week period. The HgCl2 group showed histopathological and ultrastructural lesions as evidenced by periportal fatty degeneration and cell necrosis in the liver and tubular necrosis with proteinaceous casts in the kidney. The Na2SeO4 group showed the most severe depression of growth and food and water consumption, but no pathological changes were seen in the liver or kidney. Simultaneous administration of both toxicants produced a protective effect on weight loss and histopathology. These effects were associated with the formation of electron dense nuclear inclusions in kidney proximal tubule cells and similar electron dense formations in the reticuloendothelial cell cytoplasm and in the extracellular space of Disse in the liver. These formations were shown to contain both Se and Hg by energy dispersive X-ray microanalysis. The basis of the protective interaction of these two elements appears to result from an alteration of the chemical form or association of the mercury and selenium.
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PMID:Effects of separate and combined chronic mercuric chloride and sodium selenate administration in rats: histological, ultrastructural, and x-ray microanalytical studies of liver and kidney. 54 21

Linseed meal has previously been reported to contain an organic factor that reduces toxicity of selenium in animals. The purpose of the studies reported here was to obtain information on the mechanism of action of the linseed meal factor in counteracting selenosis in chicks. Feeding a diet containing 20% linseed meal to chicks partially counteracted the growth depression caused by including high levels of selenium (10-40 ppm) in the diet. In contrast to the rat, chicks fed diets containing selenium did not accumulate significantly more of the element per unit of liver dry matter when the diet contained linseed meal, and at two selenium levels accumulated significantly less. Linseed meal did not interfere with the absorption of an oral dose of 75Se as measured by tissue retention 24 hours later. A methanol extract of linseed meal did not interfere with the normal increase in plasma glutathione peroxidase activity in chicks fed diets supplemented with low levels of selenium even though the extract counteracted the growth depression obtained by adding 20 ppm selenium. Linseed meal contains a factor that interacts with selenium in the tissues in some unknown way to reduce the toxic effects of the element, but does not prevent normal synthesis of glutathione peroxidase.
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PMID:Selenosis, hepatic selenium accumulation, and plasma glutathione peroxidase activity in chicks as affected by a factor in linseed meal. 57 18

Sulphur, selenium and nitrogen metabolism were studied in Merino wethers fed for 35-day periods on semipurified diets in which the sulphur content was increased to either 0-07 or 0-20% by the addition of sodium sulphate. At both levels of sulphur, additions of selenium as DL-selenomethionine increased the basal level of selenium (0-02 microgram/g) to 0-06, 0-09 and 0-67 microgram/g. Both levels of dietary sulphur supported positive sulphur balances but a reduction in sulphur intake per se resulted in a significant depression in dry matter digestibility (P less than 0-05), apparent nitrogen digestibility (P less than 0-05), nitrogen balance (P less than 0-01), sulphur balance (P less than 0-05) and plasma sulphate-sulphur (P less than 0-05) and wool (P less than 0-01) selenium levels. Selenium balance was not affected by differences in sulphate-sulphur intake. Selenium balances (P less than 0-001), plus the selenium levels in plasma (P less than 0-001), and wool (P less than 0-001) were significantly different at the different levels of selenium supplementation. A positive selenium balance was achieved when the selenium intake was approximately 37 microgram/day, regardless of sulphur treatment. The validity of using plasma and/or wool selenium levels as indices of the selenium status of sheep is questioned.
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PMID:Sulphur-selenium studies in sheep. I. The effects of varying dietary sulphate and selenomethionine on sulphur, nitrogen and selenium metabolism in sheep. 90 7

Four weanling swine fed for 4 weeks a commercial ration adequate in selenium and vitamin E, but supplemented with 0.5% silver acetate, developed lesions typical of selenium-vitamin E deficiency. Clinically, the pigs fed this high level of silver had anorexia, diarrhea, and growth depression; 3 of 4 pigs died. At necropsy, hepatic lesions of hepatosis dietetica were present in 4 of 4 silver-fed pigs, and 1 of 4 pigs had cardiac and skeletal muscle lesions characteristic of selenium-vitamin E deficiency. Development of lesions and mortality was prevented in 2 pigs fed the silver diet supplemented with alpha-tocopherol (100 IU/kg of diet), but not in 2 pigs fed the ration supplemented with selenium as selenite (1 ppm). Four pigs fed a lower dose level of silver (0.2% silver acetate) for 6 weeks failed to develop clinical or pathologic features of selenium-vitamin E deficiency. However, hepatic selenium content was significantly increased in pigs fed the silver-supplemented ration.
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PMID:Induction of lesions of selenium-vitamin E deficiency in pigs fed silver. 99 68

Eight 5-to 8-week-old Beagle pups were allotted to 4 groups of 2 dogs each. For 55 to 70 days, they were fed either a semisynthetic basal diet (BD) deficient in vitamin E and selenium (Se) (group 1) or the BD supplemented with either 30 IU alpha-tocopherol/kg (group 2), 0.5 ppm Se as selenite (group 3), or 1.0 ppm Se as selenite (group 4). In the dogs fed the BD, clinical signs of vitamin E-Se deficiency developed after 40 to 60 days. These signs were accompanied by increased plasma activity of creatine phosphokinase (CPK) and glutamic oxalacetic transaminase (GOT). The dogs were euthanatized after 10 to 15 days of progressive clinical signs, including muscular weakness, subcutaneous edema, anorexia, depression, dyspnea, and eventual coma. Gross lesions seen at necropsy included ventral subcutaneous edema, generalized skeletal muscular pallor and edema with scattered white longitudinal streaking, prominent brownish yellow discoloration of the intestinal musculature, and a layer of white chalky material at the renal corticomedullary junction. Microscopically, there was evidence of extensive skeletal muscular degeneration and regeneration, focal subendocardial necrosis in the ventricular myocardium, intestinal lipofuscinosis, and renal mineralization. Mean hepatic Se content in the dogs fed the BD was 0.10 ppm (wet weight basis) at necropsy. In the dogs fed the 3 supplemented diets, clinical signs of deficiency did not develop. At necropsy, mild skeletal myopathy was evident histologically in the dogs fed BD and 0.5 ppm Se (group 3) but not in the dogs fed the other supplemented diets. Intestinal lipofuscinosis was found in the dogs fed the 3 supplemented diets but was less severe in the dogs fed the diet supplemented with vitamin E than in those fed diets supplemented with Se.
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PMID:Experimentally induced vitamin E-selenium deficiency in the growing dog. 112 Jul 35

Studies were conducted to determine the effects of high levels of dietary silver nitrate and copper sulfate on the response of chicks to toxic levels of dietary selenium. Adding 5 ppm or more selenium to a basal stock diet significantly reduced growth rate, and 40 ppm or high significantly increased mortality during the 2-week experiments. Deitary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium. Hepatic selenium reached a maxiumum in chicks fed the basal diet with 10 ppm dietary selenium. Hepatic selenium of chicks fed silver was less than that of the control chicks when diets containing 10 ppm or less selenium were fed. Adding copper to the diet resulted in considerable accumulation of selenium in the liver, which was evident even at the lower levels of added selenium. Rseults of an experiment to determine the effects of deitray silver and copper on the distribution of 75-Se administered either orally or in tramusculary showed that silver interfered with absorption of selenium. The results of these experiments suggest that silver modifies selenium toxity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.
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PMID:Modification of a selenium toxicity in chicks by dietary silver and copper. 114 4

Two experiments were conducted with chicks to compare the effectiveness of vitamin E,selenium and cystine in preventing the deleterious effects of dietary silver. Adding 900 p.p.m. silver to a diet marginal in vitamin E and selenium significantly depressed growth and caused a high mortality during the four-week experiment. Most of the mortality was due to exduative diathesis. Including either 1 p.p.m. selenium or 100 I.U. vitamin E per kg. in the diets with silver prevented the growth depression and mortality. Adding 0.15% cystine stimulated growth, but failed to rpevent mortality. In a second experiment, chicks were grown on the diet containing silver with and without cystine to 15 days of age, at which time approximately 50% of the chicks exhibited signs of exudative diathesis. At that time they were either continued on the same diet of fed diets supplemented with selenium or vitamin E. Both vitamin E and selenium reduced mortality during the following two-week period, but vitamin E. was more effective than selenium.
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PMID:Induced exudative diathesis in chicks by dietary silver. 115 78

In 7 rabbits fed on hyperlipidic diet (0.5% cholesterol, 5% peanut oil and 5% lard) for 4 weeks, the ventricular myocardium was tested for antioxidant defences and thiobarbituric acid reactive substances. Seven age-matched rabbits served as controls. The hearts were previously subjected to 45 min Langendorff perfusion to study coronary flow, developed tension and resting tension; coronary effluent values of CPK activity, pH and UV absorbance at 250 nm (i.e., low molecular weight ATP catabolites) were also investigated. After 4 weeks of diet, a significant rise of plasma cholesterol (P < 0.0001) and triglycerides (P < 0.0001) was observed. Total superoxide dismutase, catalase and glutathione transferase activities underwent a significant increase (P < 0.05) in the hyperlipidemic animals. On the contrary, a depression of glutathione reductase (P < 0.01) and selenium-dependent glutathione peroxidase (P < 0.01) activities, associated with decreased levels of non proteic thiol compounds (P < 0.01), was assessed. The selenium-independent glutathione peroxidase activity was not detectable in both groups. Thiobarbituric acid reactive substances levels were significantly increased in the hyperlipidemic rabbit myocardium (P < 0.01). Even though heart hemodynamics, CPK release and perfusate pH did not differ in control and experimental animals, higher 250 nm absorbance values (P < 0.05) were detected in the myocardial effluent of hyperlipidemic rabbits. In conclusion, high fat-, cholesterol-enriched diet induces an imbalance in the rabbit heart antioxidant defences, some of which are increased, whereas others are depressed, eventually resulting in enhanced myocardial lipid peroxidation. These biochemical changes are associated with higher perfusate values of UV absorbance at 250 nm, but not with significant CPK leakage or myocardial hemodynamics derangement.
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PMID:Effects of high fat-, cholesterol-enriched diet on the antioxidant defence mechanisms in the rabbit heart. 146 87

The possibility that a subclinical deficiency of the trace element selenium might exist in a sample of the British population was examined by giving a selenium supplement for 5 weeks. Using a double-blind cross-over design, 50 subjects received either a placebo or 100 mcg selenium on a daily basis. On three occasions they filled in the Profile of Moods States. A food frequency questionnaire was used to estimate the intake of selenium in the diet. Intake was associated with a general elevation of mood and in particular, a decrease in anxiety. The change in mood when taking the active tablet was correlated with the level of selenium in the diet, which was estimated from a food frequency questionnaire. The lower the level of selenium in the diet the more reports of anxiety, depression, and tiredness, decreased following 5 weeks of selenium therapy. The results are discussed in terms of the low level of selenium in the food chain in some parts of the world.
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PMID:The impact of selenium supplementation on mood. 187 72

The ability of 2 synthetic organoselenium compounds, a dimer of p-methoxybenzeneselenol (DPMBS) and benzylselenocyanate (BSC), to induce sister-chromatid exchanges (SCE) and chromosome aberrations (CA) as well as to alter the progression of the cell through mitosis has been investigated in cultured human lymphocytes. Cultures treated with the highest concentration (2.27 x 10(-5) M) of the 2 compounds exhibited about a 3-fold increase in the level of SCE and about 2-3-fold increase in the incidence of CA. In addition, the 2 selenium compounds led to an inhibition of cell proliferation as was evidenced by the depression of the proliferation rate index (PRI).
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PMID:Chromosome aberrations, sister-chromatid exchanges and cell-cycle kinetics in human peripheral blood lymphocytes exposed to organoselenium in vitro. 221 32


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