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1. Diets containing supplements of selenium (10 mg/kg as sodium selenite), copper (500 mg/kg as copper (II) sulphate) and sodium nitroprusside (SNP 300 mg/kg) as a source of cyanide, were fed singly and in all possible combinations to chicks from 14 to 35 d of age. 2. Both copper and SNP individually alleviated the growth depression caused by excess selenium but interacted adversely with one another. The effect of SNP was to decrease liver selenium but copper increased it. Despite this contrast it is suggested that both achieve their beneficial effects through influences on the fraction of liver selenium that can be reduced to volatile forms by hydrochloric acid and zinc. 3. In a second experiment the effects of diets containing additional selenium (2 mg/kg as sodium selenite or selenomethionine) with or without additional copper (100 mg/kg) or SNP (100 mg/kg) on selenium incorporation into eggs were compared. 4. SNP reduced incorporation from selenite whereas copper had no effect. However, copper reduced the incorporation from selenomethionine into protein fractions of egg white as much as SNP.
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PMID:Interactions between dietary selenium, copper and sodium nitroprusside, a source of cyanide in growing chicks and laying hens. 883 30

Mechanisms of selenium methylation and toxicity were investigated in the liver of ICR male mice treated with selenocystine. To elucidate the selenium methylation mechanism, animals received a single oral administration of selenocystine (Se-Cys; 5, 10, 20, 30, 40, or 50 mg/kg). In the liver, both accumulation of total selenium and production of trimethylselenonium (TMSe) as the end-product of methylation were increased by the dose of Se-Cys. A negative correlation was found between production of TMSe and level of S-adenosylmethionine (SAM) as methyl donor. The relationship between Se-Cys toxicity and selenium methylation was determined by giving mice repeated oral administration of Se-Cys (10 or 20 mg/kg) for 10 days. The animals exposed only to the high dose showed a significant rise of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in plasma. Urinary total selenium increased with Se-Cys dose. TMSe content in urine represented 85% of total selenium at the low dose and 25% at the high dose. The potential of Se-methylation and activity of methionine adenosyltransferase, the enzyme responsible for SAM synthesis, and the level of SAM in the liver were determined. The high dose resulted in inactivation of Se-methylation and decrease in SAM level due to the inhibition of methionine adenosyltransferase activity. To learn whether hepatic toxicity is induced by depressing selenium methylation ability, mice were injected intraperitoneally with periodate-oxidized adenosine (100 mumol/kg), a known potent inhibitor of the SAM-dependent methyltransferase, at 30 min before oral treatment of Se-Cys (10, 20, of 50 mg/kg). Liver toxicity induced by selenocystine was enhanced by inhibition of selenium methylation. These results suggest that TMSe was produced by SAM-dependent methyltransferases, which are identical with those involved in the methylation of inorganic selenium compounds such as selenite, in the liver of mice orally administered Se-Cys. Depression of selenium methylation ability resulting from inactivation of methionine adenosyltransferase and Se-methylation via enzymic reaction was also found in mice following repeated oral administration of a toxic dose of Se-Cys. The excess selenides accumulating during the depression of selenium methylation ability may be involved in the liver toxicity caused by Se-Cys.
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PMID:Mechanisms of selenium methylation and toxicity in mice treated with selenocystine. 901 May 83

Reactive oxygen species may be involved in a broad pattern of tissue injury in patients on regular hemodialysis therapy and, in fact, increasing evidence suggests that the antioxidative system is compromized in these patients. One factor contributing to this reduction of antioxidative capacity is selenium deficiency. The present investigation was undertaken to further define the extent and type of impairment of the oxygen radical scavenger system in chronic hemodialysis patients and to evaluate the impact of selenium supplementation. Twelve non-wasted patients (6 male, 6 female, mean age of 58 years) on chronic hemodialysis for a minimum of 5 months (mean 46 months) were supplemented intravenously with 400 mg selenium (as sodium selenite) thrice weekly after each hemodialysis session over 8 weeks. Blood samples were taken before the start, at intervals of 2 weeks during, and 4 weeks after termination of supplementation. Concentrations were evaluated of selenium and alpha-tocopherol in plasma and erythrocytes, of retinol and ascorbic acid in plasma, of glutathione and the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and, catalase (CAT) in erythrocytes. Lipid peroxidation endproducts were measured as malondialdehyde (MDA) in plasma. In patients on hemodialysis multiple alterations of the antioxidative system were present and the concentrations of selenium in plasma, of glutathione and the activity of GSH-Px in erythrocytes were profoundly decreased (p < 0.001). Selenium supplementation improved the selenium status of the patients, as indicated by an increase in selenium concentrations in plasma and erythrocytes and erythrocyte GSH-Px activity. Improvement in antioxidative capacity was further documented by an increase in alpha-tocopherol in erythrocytes. Plasma MDA showed a transient decrease after 6 weeks and increased activities of SOD and CAT were dampened. No effect was seen on plasma concentrations of ascorbic acid, a-tocopherol and retinol. We conclude that patients on chronic hemodialysis therapy manifest a profound depression in antioxidative potential and a selenium deficiency. Selenium supplementation improves the oxygen radical scavenger system and increases selenium concentrations in plasma and erythrocytes and the activity of selenium dependent glutathione peroxidase. Thus, selenium should also be considered for micronutrient supplementation in patients on chronic hemodialysis therapy.
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PMID:Antioxidant status in patients on chronic hemodialysis therapy: impact of parenteral selenium supplementation. 931 Nov 3

The inhibitory effect of sodium selenite on biliary secretion of methyl mercury was examined in rats. The biliary secretion of methyl mercury in rat treated with 1 mumol/kg of methyl mercury was significantly decreased by administration of selenite at doses of 0.05 mumol/kg or higher. In rats given 10 mumol/kg of methyl mercury, marked depression of biliary secretion of mercury was observed when selenite was injected at a dose of 0.2 mumol/kg. On the other hand, secretion of substantial amounts of selenium was observed when biliary secretion of mercury was depressed. When the concentration of selenium in the bile was higher than 5 nmol/ml, biliary secretion of mercury was markedly depressed independently of the dose of methyl mercury administered (1 mumol/kg or 10 mumol/kg). These results suggest that the degree of inhibitory effect of selenite may be determined by the selenium concentration in the liver or the bile after treatment with selenite rather than the molar ratio of the dose of methyl mercury and selenite. We concluded that the decrease in biliary secretion of methyl mercury induced by selenite may result from inhibition of pathway for secretion of methyl mercury from liver to bile rather than the direct formation of a complex between methyl mercury and selenium. Methyl mercury has been considered to be secreted from liver to bile as a complex with glutathione (GSH). However, administration of selenite did not affect biliary secretion of GSH or hepatic glutathione S-transferase activity. Moreover, gel filtration of liver cytosol demonstrated that the distribution pattern of hepatic methyl mercury between macromolecules and GSH was not significantly changed by administration of selenite. These results suggest that selenite does not affect complex formation of methyl mercury with GSH at least in the liver. Selenite might specifically inhibit the activity of the canalicular transporter(s) which transport complexes of methyl mercury and GSH from the liver to bile.
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PMID:Inhibitory effect of selenium on biliary secretion of methyl mercury in rats. 936 60

The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg-1 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg-1 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.
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PMID:Effect of selenium on vanadium toxicity in different regions of rat brain. 949 34

A field investigation conducted by the South Dakota Animal Disease Research and Diagnostic Laboratory suggested that subclinical selenium toxicosis in pregnant cows may have contributed to an outbreak of aborted/stillborn calves in a high-selenium region of South Dakota. This study was undertaken to evaluate the relationship between abortion and subclinical selenium toxicosis in the dam and to assess the effects of subclinical selenium toxicosis on the bovine immune system. Fifteen pregnant cows were fed diets containing 0.25 (control), 6.0, and 12.0 ppm selenium beginning at 80-110 days gestation. Although selenium toxicosis has been reported to cause abortion, this study failed to reproduce abortions. A single cow in the 12-ppm selenium treatment group gave birth to a weak calf, which subsequently died. This calf had myocardial lesions consistent with those described for selenium toxicosis and had hepatic selenium levels of 9.68 ppm (wet weight). Elevated dietary selenium resulted in the depression of several leukocyte function parameters in pregnant cows. A statistically significant depression in forced antibody response was identified in both selenium-supplemented groups. A significantly diminished mitogenic response to concanavalin A and pokeweed mitogen was also observed in the 12-ppm selenium group. Although a similar pattern of depression was also observed with phytohemagglutinin, differences were not significant. These findings indicate that even in the absence of clinical alkali disease, elevated selenium levels may adversely affect both pregnancy outcome and the bovine immune system.
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PMID:The effect of subclinical selenium toxicosis on pregnant beef cattle. 968 76

The 4 natural oxidation states of selenium are elemental selenium (0), selenide (-2), selenite (+4), and selenate (+6). Inorganic selenate and selenite predominate in water whereas organic selenium compounds (selenomethionine, selenocysteine) are the major selenium species in cereal and in vegetables. The principal applications of selenium include the manufacture of ceramics, glass, photoelectric cells, pigments, rectifiers, semiconductors, and steel as well as use in photography, pharmaceutical production, and rubber vulcanizing. High concentrations of selenium in surface and in ground water usually occur in farm areas where irrigation water drains from soils with high selenium content (Kesterson Reservoir, California) or in lakes receiving condenser cooling water from coal-fired electric power plants (Belews Lake, North Carolina). For the general population, the primary pathway of exposure to selenium is food, followed by water and air. Both selenite and selenate possess substantial bioavailability. However, plants preferentially absorb selenates and convert them to organic compounds. Aquatic organisms (e.g., bivalves) can accumulate and magnify selenium in the food chain. Selenium is an essential component of glutathione peroxidase, which is an important enzyme for processes that protect lipids in polyunsaturated membranes from oxidative degradation. Inadequate concentrations of selenium in the Chinese diet account, at least in part, for the illness called Keshan disease. Selenium deficiency occurs in the geographic areas where Balkan nephropathy appears, but there is no direct evidence that selenium deficiency contributes to the development of this chronic, progressive kidney disease. Several lines of scientific inquiry suggest that an increased risk of cancer occurs as a result of low concentrations of selenium in the diet; however, insufficient evidence exists at the present time to recommend the use of selenium supplements for the prevention of cancer. The toxicity of most forms of selenium is low and the toxicity depends on the chemical form of selenium. The acute ingestion of selenious acid is almost invariably fatal, preceded by stupor, hypotension, and respiratory depression. Chronic selenium poisoning has been reported in China where changes in the hair and nails resulted from excessive environmental exposures to selenium. Garlic odor on the breath is an indication of excessive selenium exposure as a result of the expiration of dimethyl selenide. The US National Toxicology Program lists selenium sulfide as an animal carcinogen, but there is no evidence that other selenium compounds are carcinogens.
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PMID:Selenium. 1038 53

Astragalus lusitanicus is a toxic legume grown in Morocco and in some other Mediterranean countries. In small ruminants, poisoning by this plant is dominated by nervous signs characterized by many cycles of excitement-depression. Macroscopic examination of poisoned animals showed congestive lesions and oedema in the brain and lungs. Microscopic lesions consisted mainly of vacuolar degeneration in neurons, hepatocytes and in spleen and kidney cells. Serum activity of AST and CK as well as blood glucose and urea were increased as a result of poisoning. However, serum activity of alpha-mannosidase was not modified as is the case in locoism. Chemical investigations showed that A. lusitanicus does not contain swainsonine or miserotoxin and its selenium concentration is very low. However, this legume contains indolizidin alkaloids and a first compound was purified and identified.
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PMID:Toxicology of Astragalus lusitanicus Lam. 1070 44

To gain insight into the biochemical mechanisms of organotin toxicity, the effects of oral subchronic exposure (70 d) to triphenyltin acetate (TPTA) on hepatic and renal enzymes involved in glutathione metabolism were investigated in rabbits and lambs. Rabbits were offered a diet fortified with 15, 75 or 150 ppm TPTA, whereas lambs were daily given 1 or 7.5 mg/kg TPTA On the whole, rabbits were more susceptible than lambs and in both species hepatic enzymes were affected to a greater extent than renal enzymes. In rabbit liver, glutathione S-transferase activity toward 1,2-dichloro-4-nitrobenzene (DCNB) was enhanced at 15 ppm and depressed at 150 ppm TPTA, whereas selenium-dependent glutathione peroxidase (Se-GPX) decreased in a dose-related manner; glyoxalase II (GII) activity increased to the same extent at 15 or 75 ppm TPTA but was unaffected at 150 ppm TPTA. For renal enzyme activities in rabbits, only GPX activity was significantly inhibited at 150 ppm TPTA. The only statistically significant changes in lambs were a fall in both hepatic GST accepting DCNB as substrate at 7.5 mg/kg and Se-GPX at 1 or 7.5 mg/kg TPTA, and an increase in renal GII activity at 7.5 mg/kg TPTA. These results suggest that depression of important antioxidant enzymes such as GST and GPX are part of the complex mechanism of organotin toxicity.
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PMID:Changes in hepatic and renal glutathione-dependent enzyme activities in rabbits and lambs subchronically treated with triphenyltin acetate. 1083 20

The need exists for compounds that will protect individuals from high-dose acute radiation exposure in space and the agents that might be less protective but less toxic and longer acting. Metals and metal derivatives provide a small degree of radioprotection (dose reduction factor < or = 1.2 for animal survival after whole-body irradiation). Emphasis is placed here on the radioprotective potential of selenium (Se). Both the inorganic salt, sodium selenite, and the organic Se compound, selenomethionine, enhance the survival of irradiated mice (60Co, 0.2 Gy/min) when injected IP either before (-24 hr and -1 hr) or shortly after (+15 min) radiation exposure. When administered at equitoxic doses (one-fourth LD10; selenomethionine = 4.0 mg/kg Se, sodium selenite = 0.8 mg/kg Se), both drugs enhanced the 30-day survival of mice irradiated at 9 Gy. Survival after 10-Gy exposure was significantly increased only after selenomethionine treatment. An advantage of selenomethionine is lower lethal and behavioral toxicity (locomotor activity depression) compared to sodium selenite, when they are administered at equivalent doses of Se. Sodium selenite administered in combination with WR-2721, S-2-(3-aminopropylamino)ethylphosphorothioic acid, enhances the radioprotective effect and reduces the lethal toxicity, but not the behavioral toxicity, of WR-2721. Other studies on radioprotection and protection against chemical carcinogens by different forms of Se are reviewed. As additional animal data and results from human chemoprevention trials become available, consideration also can be given to prolonged administration of Se compounds for protection against long-term radiation effects in space.
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PMID:Radioprotection by metals: selenium. 1153 12


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