Showing papers on "Selenium published in 1975"

Correlation between selenium and mercury in man following exposure to inorganic mercury

Abstract: THE ability of selenium compounds to modify profoundly the toxicity of both organic and inorganic mercury compounds has been demonstrated in experimental animals by Parizek and co-workers1,2. The analytical data of Ganther et al.3 on tuna and of Koeman et al.4 on marine mammals showed that natural levels of mercury and selenium are strongly correlated. Here we report an approximately molar ratio for these elements in certain human organs following exposure to high levels of inorganic mercury.

Biochemical function of selenium and its relation to vitamin E.

Abstract: Glutathione peroxidase (glutathione:H2O2 oxidoreductase, E.C. 1.11.1.9), isolated from ovine and bovine erythrocytes, has recently been shown to contain 4 selenium atoms per mole, an average of 1 Se per protein subunit of about 22,000 molecular weight. Selenium deficiency in the rat, chick and sheep causes dramatic decreases in the activity of this enzyme in the tissues, but certain sites such as liver are affected more than others. Decreases in glutathione peroxidase correlate with lesions caused by selenium deficiency and appear useful in diagnosing selenium deficiency. Glutathione peroxidase is an important enzyme in destroying H2O2 and organic hydroperoxides such as lipid hydroperoxides. It therefore guards against oxidative damage to the cell membranes and other oxidant-sensitive sites in the cell. While this selenium-dependent system destroys lipid hydroperoxides and other peroxides, vitamin E is believed to protect against oxidant damage to membranes by preventing the formation of lipid hydroperoxides. A scheme is proposed, based on oxidant damage and its prevention, which accounts for the interaction between selenium, vitamin E, unsaturated lipids, sulfur-containing amino acids, and cell damaging agents such as oxidant stressors and toxicants such as silver and tri-o-cresyl phosphate. The background for such a scheme is reviewed.

Acid-volatile selenium formation catalyzed by glutathione reductase.

Abstract: The production of acid-volatile selenide (apparently H2Se) was catalyzed by glutathione reductase in an anaerobic system containing 20 mM glutathione, 0.05 mM sodium selenite, a TPNH-generating system, and microgram quantities of highly purified yeast glutathione reductase. H2Se production in this system was proportional to glutathione reductase concentration and was maximal at pH 7. Significant nonenzymic H2Se production occurred in the system lacking glutathione reductase and TNPH. A concentration of arsenite (0.1 mM) which does not inhibit glutathione reductase inhibited selenide volatilization, as did bovine serum albumin (1.67 mg/ml). Both appear to inhibit Se volatilization by reacting with the selenide product(s). The selenotrisulfide derivative of glutathione (GSSeSG) was readily converted to H2Se by glutathione reductase and TPNH without the addition of glutathione. These results suggest that GSSeSG formed nonenzymically from glutathione and selenic undergoes stepwise reduction by glutathione reductase (or excess GSH) to GSSeH and finally to H2Se. The same pathway operates when glutathione is used as the reducing agent but to a lesser extent.

Selenium Levels in Human Blood and Tissues in Health and in Disease

Abstract: The levels of selenium in human sera and pancreatic, hepatic and synovial tissues were measured. An attempt was made to correlate the selenium level with certain disease states. Selenium was determined by nerutron activation analysis, using the 17.4 second half-life isotope 77mSe with a sensitivity of 2ppb. Serum-bound selenium was determined in normal individuals and individuals with various malignancies, and medical and surgical disorders. Tissue selenium was assayed in diseased and normal pancreases, livers, and synovial membranes. A wide variation was observed both in the serum selenium content of patients with a malignancy and in postmoren pancreatic and synovial showing histopathological changes. Significantly lower selenium values were observed in sera from cancer patients than from normal individuals. Higher values were generally observed in patients with primary neoplasms of the reticuloendothelial system. Higher tissue concentrations were obtained in synovia from patients with rheumatoid arthritis and in pancreatic tissues associated with histopathological changes.

Selenium content of food consumed by Canadians.

Abstract: Four composite diets from three cities, each representing the daily per capita consumption of foods in Canada, contained on analysis 191, 220, 113, and 150 mug selenium. Cereals provided the most selenium (62-112 mug) followed by meat, poultry, and fish (25-90 mug) and dairy products (5-25 mug). The average daily intake of selenium in Canada was also calculated from published analytical data and the per capita disappearance of unprepared foods. The total intake was 197 mug/day, and the major sources were wheat flour (98 mug), pork (21 mug), poultry products (24 mug), and fish (17 mug). Because the average diet is rich in selenium, the possibility of a deficiency in the adult is considered to be remote. Milk is relatively low in selenium, and thus the greatest deprivation in humans would occur during infancy.

The Copper–Selenium System at Temperatures to 850 K and Pressures To 50 Kbar

Abstract: Phase relationships in the copper/selenium system in the composition range 30–70 atomic % selenium have been studied at temperatures from 298 to 850 K and at pressures to 50 kbar. A revised atmosph...

Mechanisms of action of selenium and vitamin E in protection of biological membranes.

Abstract: Opinions vary as to the mode of action of vitamin E and selenium. Some argue that they act as nonspecific biological antioxidants. Others propose that the functions of the two substances are distinct and that vitamin E acts as a true vitamin in addition to functioning as a lipid-soluble antioxidant. Support for the "Biological Antioxidant Theory" is largely circumstantial. However, lipoperoxides have been detected in adipose tissues of vitamin E-deficient animals, and increased rates of in vitro peroxidation have been demonstrated in homogenates of several tissues of selenium and vitamin E-deficient animals. The basis of the antioxygenic role of selenium in these systems was elucidated by the discovery of Rotruck et al. (1973) that selenium is a component of rat erythrocyte glutathione peroxidase. Further studies in this laboratory have demonstrated the important role of glutathione peroxidase in protection against the vitamin E- and selenium-deficiency disease of chicks, exudative diathesis, which results from increased capillary permeability. Also shown were the activities of both dietary selenium and vitamin E in prevention of ascorbate-induced peroxidation in mitochondrial and microsomal preparations from chick liver. Recent results demonstrate that both selenium and vitamin E are required to protect hepatic mitochondria and microsomes from peroxidative degradation. Dietary requirements of the chick for both nutrients for this function have been determined: approximately 0.06 ppm selenium in the presence of adequate vitamin E; 30-50 IU vitamin E per kg in the presence of adequate selenium.

Modification of a selenium toxicity in chicks by dietary silver and copper

Abstract: 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 higher significantly increased mortality during the 2-week experiments Dietary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium Hepatic selenium reached a maximum 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 Results of an experiment to determine the effects of dietary silver and copper on the distribution of /sup 75/Se administered either orally or intramuscularly showed that silver interfered with absorption of selenium The results of these experiments suggest that silver modified selenium toxicity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in themore » tissues Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues« less

Geographic Distribution of Selenium in Human Milk

Abstract: Data were collected on the selenium concentration in human mature milk from a total of 241 subjects who resided in or near cities located in 17 states across the United State. The overall mean value for the selenium content of mature human milk was 0.018 ppm Se. Most of the individual values for selenium in human milk fell within the narrow range of 0.007 to 0.033 ppm Se, yet there was evidence for geographic variations in the selenium content of milk collected from the various cities.

The atomic-fluorescence determination of antimony, arsenic, selenium and tellurium by using the hydride generation technique

Abstract: The method of determination of antimony, arsenic, selenium and tellurium, by using a sodium borohydride reduction with subsequent atomic fluorescence, was found to be very sensitive.The calibration graphs were linear over a wide range of concentrations and the method was 5–30 times more sensitive than the corresponding atomic-absorption technique.

A tentative recommendation for the maximum daily intake of selenium.

Abstract: In order to make a tentative recommendation for the maximum acceptable daily intake of selenium, relevant data were compiled from the available literature. Normal daily intake of selenium from foods was estimated as about 100 mug, half of which comes from fish and shellfish (in an average adult Japanese). Intake of selenium from other sources was negligible. The amount of selenium excreted in the urine was found to be compatible with the estimated value of the daily oral intake. The range of the margin of safety was then estimated as 10 to 200 times the normal level on the basis of human and animal toxicity data. The variation of dietary selenium intake in the general population is discussed, leading to the conclusion that the consumers of large amounts of fish may ingest as much as 500 mug daily. Consequently, a value of 500 mug is proposed as the tentative maximum acceptable daily intake of selenium for the protection of human health.

Interrelationships of selenium with other trace elements.

Abstract: Biological interactions between selenium and a number of other elements occur that render selenium much less toxic than when it is present alone. These elements are arsenic, mercury, cadmium, and copper. Furthermore, the presence of selenium reduces the toxicity of mercury and cadmium. These are general biological interactions and have been found to occur in a number of animal species under a variety of conditions. It has been shown that the reaction products of selenium with mercury and cadmium are less toxic than an equal amount of selenium fed alone to chicks. The presence of arsenic shifts the excretion of selenium to the bile. There is no conclusive evidence that the presence of other elements reduces the absorption or retention of selenium. It is possible that some of the interactions are caused by the formation of a compound by selenium and other elements which has less affinity for active groups on biologically active compounds.--Hill, C.H. Interrelationships of selenium with other trace elements.

Precipitation of a selenium deficiency by high dietary levels of copper and zinc.

Abstract: High mortality and a high incidence of exudative diathesis and muscular dystrophy were observed in chicks fed a diet supplemented with either 800 or 1600 ppm copper. Adding 0.5 ppm selenium to a basal diet containing 0.2 ppm prevented mortality and selenium deficiency signs. Dietary zinc levels of 2100 to 4100 ppm also resulted in high mortality, exudative diathesis, and muscular dystrophy. A selenium supplement of 0.5 ppm completely prevented the deficiency signs and markedly reduced mortality. The results demonstrate that both copper and zinc can induce a selenium deficiency in chicks when a diet relatively low in this element is fed.

Protective effect of selenium on certain hepatotoxic and pancreotoxic manifestations of subacute cadmium administration.

Abstract: Administration of cadmium chloride (1.0 mg/kg s.c.) to rats, twice a day for 7 days, significantly stimulated the activities of hepatic pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose 1,6-diphosphatase and glucose 6-phosphatase, markedly increased the concentration of hepatic cyclic adenosine monophosphate and circulating blood glucose and significantly reduced serum insulin levels. Furthermore, subacute exposure to cadmium induced glucose intolerance that was associated with a decreased pancreatic secretory activity as evidenced by lowered insulinogenic indices and marked inhibition of phentolamine-stimulated insulin release. In contrast to cadmium, administration of selenium dioxide (2 X 1.0 mg/kg/day s.c., 7 days) failed to alter significantly the activities of gluconeogenic enzymes, hepatic cyclic adenosine monophosphate, blood glucose or serum insulin levels, glucose tolerance or the pancreatic secretory activity. However, administration of selenium concurrently with cadmium completely prevented the cadmium-induced increases of hepatic gluconeogenic enzymes. Treatment with selenium ameliorated the cadmium-induced hyperglycemia, hypoinsulinemia, glucose intolerance and the suppression of pancreatic secretory activity, whereas it failed to alter significantly the cadmium-induced elevation of hepatic cyclic AMP levels. Data provide evidence suggesting that subacute exposure to cadmium alters several parameters of carbohydrate metabolism and suppresses pancreatic secretory activity and that administration of selenium alone is without any appreciable effect on the above parameters. However, administration of selenium concurrently with cadmium prevents, to varying degrees, several of the cadmium-induced metabolic and functional changes.

The Chemistry and Technology of Selenium and Tellurium

Abstract: It is an unenviable task to have to select, without significant omission, a number of important papers on this topic. The 43 papers that were chosen, however, cover the subject-matter well except that there is very little on the general crystal chemistry of germanium. Special attention has been given to papers on germanium in meteorites and on meteorite classification, especially those by J. T. Wasson, published in the usually accessible Geochimica et Cosmochimica Acta. The editor's comments are short and do not add much to the value of the book. The quality of production is generally good but the reproduction of photomicrographs is barely adequate and in the reviewer's copy the pages were bound in the wrong sequence. This book is unlikely to be a strong contender for the use of library funds especially when a library already has the Handbook of Geochemistry (Min. Mag. 38, 533-4). The chapter on germanium in the latter is undoubtedly of more use for a summary of the pre-I969 literature and for its good bibliography. Weber's book has the advantage that more than twenty of the selected papers were published between I966 and ~97o and some of these are from the less accessible Russian journals. P. HENDERSON