Showing papers on "Selenium published in 1977"
TL;DR: The results support the hypothesis that selenium has cancer-protecting effects in man and a change of diet aimed at increasing the dietary selenum supply is suggested as a possible means of lowering the human cancer risk.
493 citations
472 citations
TL;DR: Selenium decreased the total number of colon tumors induced by MAM to 42 tumors as compared to a total of 73 tumors in rats receiving only MAM, while selenium at this level did not affect the weight gain of the animals.
160 citations
TL;DR: The geochemistry of selenium is largely controlled by that of iron, with which Se is closely affiliated in both oxidizing and reducing environments as mentioned in this paper, and Se oxyanions, HSeO−3 and SeO2−3, are strongly adsorbed by hydrated surfaces of ferric oxides over the pH range 2-8; above pH8 adsorption decreases to complete desorption at pH 11.
158 citations
157 citations
TL;DR: An automated solvent extraction method, based on the fluorescence of 4,5-benzopiazselenol has been developed for the determination of nanogram quantities of selenium as mentioned in this paper.
154 citations
TL;DR: Increased biliary excretion of selenium caused by arsenic provides a reasonable rationale for the ability of arsenic to counteract the toxicity of seenium, although the chemical mechanism by which arsenic does this is not certain.
Abstract: In 1938, Moxon discovered that arsenic protected against selenium toxicity. Since that time it has been shown that this protective effect of arsenic against selenium poisoning can be demonstrated in many different animal species under a wide variety of conditions. Antagonistic effects between arsenic and selenium have also been noted in teratologic experiments. Early metabolic studies showed that arsenic inhibited the expiration of volatile selenium compounds by rats injected with acutely toxic doses of both elements. This was puzzling since pulmonary excretion had long been regarded as a means by which animals could rid themselves of excess selenium. However, later work demonstrated that arsenic increased the biliary excretion of selenium. Not only did arsenic stimulate the excretion of selenium in the bile, but selenium also stimulated the excretion of arsenic in the bile. This increased biliary excretion of selenium caused by arsenic provides a reasonable rationale for the ability of arsenic to counteract the toxicity of selenium, although the chemical mechanism by which arsenic does this is not certain. The most satisfactory explanation is that these two elements react in the liver to form a detoxication conjugate which is then excreted into the bile. This is consistent with the fact that both arsenic and selenium each increase the biliary excretion of the other. Several other metabolic interactions between arsenic and selenium have been demonstrated in vitro, but their physiological significance is not clear. Although arsenic decreased selenium toxicity under most conditions, there is a pronounced synergistic toxicity between arsenic and two methylated selenium metabolites, trimethylselenonium ion or dimethyl selenide. The ecological consequences of these synergisms are largely unexplored, although it is likely that selenium methylation occurs in the environment. All attempts to promote or prevent selenium deficiency diseases in animals by feeding arsenic have been unsuccessful. Over 30 years ago it was suggested that industrial hygienists use arsenic as a tonic to prevent or cure selenium poisoning in workers exposed to this hazard. Organic arsenical feed additives were tried as partial antidotes against selenium poisoning in livestock raised in seleniferous agricultural areas but were not found to be practical.
150 citations
TL;DR: Selenium reduced the incidence of liver tumor incidence from 92% (11/12) in the Group I control, to 46% (7/15) in Group II and to 64% (9/14) in Groups III.
123 citations
TL;DR: Results of a survey of metal levels in nine species of important commercial fish from New South Wales waters are reported, finding mercury in all species sampled occurred almost entirely as methyl mercury.
Abstract: Results of a survey of metal levels in nine species of important commercial fish from New South Wales waters are reported. Muscle samples from 20-30 individuals of each species were analysed for mercury, cadmium, lead, copper and zinc. Eight to 12 individuals of each species were analysed for selenium and arsenic. Of the 232 fish analysed, 231 had concentrations of cadmium, lead, copper and zinc below the National Health and Medical Research Council (NHMRC) standards for these elements in foodstuffs. Several specimens of bream, snapper, mulloway, kingfish, Australian salmon and yellowfin tuna had total mercury concentrations in excess of the NHMRC standard of 0.5 ppm. These fish accounted for approximately 7% of the total number sampled. None of the sea mullet, flathead and tailor sampled exceeded the standard for mercury. The mercury in all species sampled occurred almost entirely as methyl mercury. Of the 95 fish analysed for arsenic and selenium, 20 fish (21 %) had arsenic concentrations equal to or greater than the NHMRC standard for selenium. The health risks associated with the presence of mercury and arsenic in these species are discussed.
122 citations
TL;DR: The selenium content of some commercially available milk formulas for infants are lower than those of human and cow's milk and the activities of the Selenium containing enzyme glutathione peroxidase of erythrocytes are reduced in early infancy.
Abstract: The selenium concentration of serum is age-dependent. The median value at birth (chi=50 X 10(-9)g/ml) amounts to half of the median value of adults (chi=102 X 10(-9)g/ml). After a decrease in early infancy to chi=34 X 10(-9)g/ml it steadily increases to chi=58 X 10(-9)g/ml in the second half of the first year, to chi=82 X 10(-9)g/ml in 1--5 year old children, and to chi=92 X 10(-9)g/ml in school children. The activities of the selenium containing enzyme glutathione peroxidase of erythrocytes are also reduced in early infancy (chi=7.2 +/- 0.36 U37/g Hb), whereas the enzyme activities of cord blood erythrocytes (chi=8.72 +/- 0.76 U37/g Hb) are in the same range as those of older children or adults. The selenium content of some commercially available milk formulas for infants are lower than those of human and cow's milk.
119 citations
TL;DR: A pathway for the synthesis of dimethyl selenide from sodium selenite was studied in rat liver and kidney fractions under anaerobic conditions in the presence of GSH, a NADPH-generating system, and S-adenosylmethionine and it was concluded that Fraction C contains a methyltransferase acting on small amounts of hydrogen selenides produced non-enzymically by the reaction of selenites with GSH.
TL;DR: Bacteria capable of utilizing trimethylselenonium, dimethyl selenide, and dimethyl diselenide as carbon sources were isolated from soil and six of 10 microorganisms able to grow on cystine used selenocystine as a sole source of carbon and formed elemental selenium, and one of the isolates, a pseudomonad, was found also to produce selenides.
Abstract: Resting cell suspensions of a strain of Corynebacterium isolated from soil formed dimethyl selenide from selenate, selenite, elemental selenium, selenomethionine, selenocystine, and methaneseleninate. Extracts of the bacterium catalyzed the production of dimethyl selenide from selenite, elemental selenium, and methaneseleninate, and methylation of the inorganic Se compounds was enhanced by S-adenosylmethionine. Neither trimethylselenonium nor methaneselenonate was metabolized by the Corynebacterium. Resting cell suspensions of a methionine-utilizing pseudomonad converted selenomethionine to dimethyl diselenide. Six of 10 microorganisms able to grow on cystine used selenocystine as a sole source of carbon and formed elemental selenium, and one of the isolates, a pseudomonad, was found also to produce selenide. Soil enrichments converted trimethylselenonium to dimethyl selenide. Bacteria capable of utilizing trimethylselenonium, dimethyl selenide, and dimethyl diselenide as carbon sources were isolated from soil.
TL;DR: Balances of twenty trace elements have been determined in four male patients during total parenteral nutrition including fat emulsion and a special solution for addition of Fe, Zn, manganese, Cu, fluorine and iodine, besides calcium and magnesium, to the infusion solutions.
Abstract: 1. Balances of twenty trace elements (silver, arsenic, gold, bromine, cadmium, cobalt, chromium, caesium, copper, iron, mercury, lanthanum, molybdenum, rubidium, antimony, scandium, selenium, samarium, tungsten and zinc) have been determined in four male patients during total parenteral nutrition incliding fat emulsion and a special solution for addition of Fe, Zn, manganese, Cu, fluorine and iodine, besides calcium and magnesium, to the infusion solutions. 2. The analyses for trace elements were made with the aid of an ion-exchange technique based on neutron activation, and combined with subsequent gamma spectrometry. 3. The intended intravenous supply of trace elements correspond approximately to the analysed supply. However, all the other trace elements determined were found to be unintentionally administered in small amounts. 4. There was a substantial retention of Fe. Other elements retained were Ag, Co, Cr, Cu, Sb, Sc, and W. 5. Particularly Br and Rb were lost by the patients, but negative balances were also found for As, Au, Cd, Cs, Mo, Se and Zn. However, Zn was retained by one patient with short bowel syndrome. 6. The serum concentrations of thirteen (Ag, Br, Co, Cs, Cu, Fe, Hg, Mo, Rb, Sc, Se, W and Zn) of the trace elements were found to have some decrease during the period of total parenteral nutrition, mostly in accordance with the corresponding balance values, Fe, in particular, was found to have the derectional change in concentration. 7. The administration of trace elements is recommended in long-term total parenteral nutrition.
TL;DR: In this article, the results suggest metabolic involvement in the uptake and long distance transport of solenium supplied as selenite, despite lower Se concentrations in the xylem exudate than in the external solution.
Abstract: Selenate and selenite transport through tomato root systems were followed for periods up to 4 h after removal of the plant tops, using Se as a tracer.With selenate, Se concentrations in the xylem exudate were 6 to 13 times higher than in the external solution, and chromatographic analysis showed that the selenium was transported as inorganic selenate (SeO42-).With selenite, Se concentrations in the exudate were always lower than in the external solution. Analyses of exudate samples showed that negligible amounts of selenium were transported as inorganic selenite (HSeO3-except at very high external selenite concentrations (500 μM), when up to 7 per cent was transported as selenite. Most of the selenium transport in selenite-fed plants was as selenate or as an unknown selenium compound, the relative proportions of these two forms varying both with time and with external selenite concentration. Addition of a 5-fold excess of sulphate over selenite had no detectable effect on the concentrations of selenate in the exudate, but caused substantial decreases in the maximum concentrations of both total selenium (c. 47 per cent decrease) and the unknown selenium compound (c. 69 per cent decrease). Addition of a 5-fold excess of sulphite decreased the concentration of the unknown (c. 39 per cent) but caused a large (2.7-fold) increase in the maximum total selenium concentration in the exudate and a 7.9-fold increase in the maximum concentration of selenate. The results suggest metabolic involvement in the uptake and long distance transport of solenium supplied as selenite, despite lower Se concentrations in the xylem exudate than in the external solution. An attempt is made to incorporate the new and existing information into a selenium transport model.
TL;DR: Evidence is presented that selenite can release methylmercury from its linkage with proteins and thereby influence its tissue distribution and that inorganic selenium prevents growth inhibition as well as mortality and neurotoxicity due to methylMERcury given simultaneously in the diet of Japanese quail and rats.
Abstract: SINCE Parizek et al.1 reported that administration of selenite clearly decreased toxicity of mercuric chloride, there have been many studies on the mechanisms responsible for the interrelationship between selenium and inorganic or organic mercury. Almost all have shown that inorganic selenium, especially selenite, prevents growth inhibition as well as mortality and neurotoxicity due to methylmercury given simultaneously in the diet of Japanese quail2–4 and rats5–8. Protective effects of selenium against methylmercury toxicity do not involve mercury absorption through intestines9 or excretion in the urine and faeces6. Selenite does not increase the rate of breakdown of methylmercury7, and thionein does not have a significant role in the detoxification of methylmercury3, but presumably, the form of methylmercury is modified in some way by selenium. We present here evidence that selenite can release methylmercury from its linkage with proteins and thereby influence its tissue distribution.
TL;DR: Selenium can be determined quantitatively in biological samples after nitric acid-magnesium nitrate digestion and formation of 5-nitropiazselenole, by extraction into toluene for gas-liquid chromatography with electron-capture detection.
TL;DR: Tissue accumulation, subcellular incorporation and soluble protein binding of 203Hg and 75Se in the liver and kidney were studied and PMA and MMC gave different changes suggesting that their interactions with selenite were indeed complex.
TL;DR: The distribution of mercury and selenium has been examined in subcellular fractions of rat liver and kidneys in prolonged exposure to HgCl2 and Na2SeO3 administered separately and simultaneously.
Abstract: The distribution of mercury and selenium has been examined in subcellular fractions of rat liver and kidneys in prolonged exposure to HgCl2 and Na2SeO3 administered separately and simultaneously The molar ratio of mercury and selenium concentrations in subcellular fractions of the organs examined varied considerably Selenium displaced mercury from the soluble kidney fraction bound mainly with metallothionein to the nonhistone protein fraction of liver nuclei The Hg-stimulated biosynthesis of metallothionein has been eliminated under the influence of selenium
TL;DR: It is concluded that ATP sulphurylase can catalyse the formation of adenosine 5'-selenophosphate and can explain the ability of mammals, lacking a sulphate reductase system, to incorporate selenium from selenate into seleno-amino acids.
Abstract: In the presence of ATP and Mg2+, ATP sulphurylase from Saccharomyces cerevisiae catalysed the conversion of selenate into a compound with the electrophoretic and acid-lability properties of adenosine 5′-sulphatophosphate. Structural characterization, involving extensive purification of adenosine 5′-selenophosphate, proved impossible. However, we showed ATP-, Mg2+- and ATP sulphurylase-dependent, and inorganic pyrophosphatase-stimulated, production of elemental selenium from selenate in the presence of GSH (reduced glutathione). Since selenate was not reduced by GSH, this reaction proved that ATP sulphurylase had formed an active selenate. The enzyme catalysed formation of elemental selenium had the same kinetics and GSH-dependency as the non-enzymic reduction of selenite to elemental selenium by GSH. In the presence of inorganic pyrophosphatase, 2 mol of Pi was released for each mol of ‘active selenate’ formed. This was shown by a spectrophotometric assay for elemental selenium. The observed reactivity with thiols and the instability of the enzymic product were those predicted for selenium anhydrides. By analogy with the chemistry of sulphur, the product of the thiolytic cleavage of a selenium anhydride would be converted into selenite. The selenite would then be reduced by the thiol to elemental selenium. We conclude that ATP sulphurylase can catalyse the formation of adenosine 5′-selenophosphate. The anhydride can be reduced by thiols in a manner similar to the reduction of selenite. These results probably explain the ability of mammals, lacking a sulphate reductase system, to incorporate selenium from selenate into seleno-amino acids.
TL;DR: Evidence is presented to suggest that 0.1 ppm dietary selenium is not sufficient under some conditions to meet the physiological requirements for this element.
Abstract: The effects of selenium and vitamin E on blood selenium levels and tissue glutathione peroxidase activities were determined in sheep fed purified and hay diets. A significant increase of blood levels of this element and tissue glutathione peroxidase activities was found in sheep given selenium as compared to those not receiving this element. Of the tissues examined, the highest glutathione peroxidase activity was found in the heart. Vitamin E had no influence on either the blood selenium levels or upon the tissue glutathione peroxidase activity. With hydrogen peroxide as the substrate, tissue glutathione peroxidase activity was not correlated with the incidence of white muscle disease. Evidence is presented to suggest that 0.1 ppm dietary selenium is not sufficient under some conditions to meet the physiological requirements for this element.
TL;DR: The iron, zinc, selenium, rubidium, and cesium concentrations in serum and packed blood cells were determined by instrumental neutron activation analysis without chemical separations.
Abstract: We determined the iron, zinc, selenium, rubidium, and cesium concentrations in serum and packed blood cells by instrumental neutron activation analysis without chemical separations. Lyophilized samples were irradiated for 12 days at a flux of 10(13) neutrons-cm-2-s-1, mineralized by wet digestion, and measured two times with a high-resolution Ge(Li) detector--for 6 h about a month after the irradiation and for 15 h two or three months after the irradiation, The following values were obtained: 163 +/- 0.43 mg/liter (serum iron), 1025 +/- 136 mg/kg wet wt (packed cells iron), 1? +/- 0.20 mg/liter (serum zinc), 11.15 +/- 1.83 mg/kg wet wt (packed cells zinc), 0.13 +/- 0.02 mg/liter (serum selenium), 0.16 +/- 0.03 mg/kg wet wt (packed cells selenium), 0.17 +/- 0.04 mg/liter (serum rubidium), 4.28 +/- 0.98 mg/kg wet wt (packed cells rubidium), 0.74 +/- 0.20 microgram/liter (serum cesium), and 4.82 +/- 2.10 microgram/kg wet wt (packed cells cesium).
TL;DR: The effect of combined supplementation with selenium and Vitamin E upon fertilization of ova was evaluated in beef cattle maintained on either an adequate or inadequate nutrition.
TL;DR: Twenty-four h after the subcutaneous administration of 0.5 μmoles selenite labelled with 75Se to rats of 200 g body weight, the retention of selenium at the injection site was significantly increased by the presence of equimolar amounts of methylmercury in the injection solution.
Abstract: Twenty-four h after the subcutaneous administration of 0.5 μmoles selenite labelled with 75Se to rats of 200 g body weight, the retention of selenium at the injection site was significantly increased by the presence of equimolar amounts of methylmercury in the injection solution. The retention of Me203HgCl was not affected by the presence of selenite. The most significant shift caused by interaction was a decrease in the blood content and an increase in the brain content of 203Hg. The brain content of 75Se was also increased to a lesser extent. The shift in the distribution — which was the same whether the two metals were injected at the same site or separately — continuously decreased from 6–48 h. The same interaction pattern was observed when methylmercury and selenite were administered by gastric gavage and differences in distribution increased when the dose was increased from 1.25 μmoles/kg to 2.5 μmoles/kg. The increase in the brain content of mercury caused by selenite was not restricted to simultaneous administration and occurred when selenite was given 2–7 days after methylmercury.
TL;DR: Selenium (Se) inhibition of either the activation of test compounds and/or mutagenic events elicited by activated compounds is suggested by experimental rat assay, mutagenesis assays, and assays with human lymphocytes in culture.
Abstract: Selenium (Se) inhibition of either the activation of test compounds and/or mutagenic events elicited by activated compounds is suggested by experimental rat assays, mutagenesis assays, and assays with human lymphocytes in culture. The colon tumor incidence in 1,2-dimethylhydrazine (DMH)-treated rats was reduced from 87% to 40% by 4 ppm Se supplements in the drinking water. Supplemental Se decreased the total number of colon tumors induced by DMH more than three-fold and by methylazoxymethanol (MAM) almost two-fold. Coexposure of Salmonella typhimurium TA 1538 to an effective molar ratio of Se/2-acetylaminofluorene=10, Se/N-OH-acetylaminofluorene=10 and SE/N-OH-aminofluorene=300 reduced the mutagenicity to 65, 68, and 61% of their respective controls with mutagen alone. With a molar ratio of Se/N-OH-AAF=100, Se reduced the activity to 28% of the mutagenicity of N-OH-AAF alone. Preliminary data indicating MAM is mutagenic in S. typhimurium TA 1535 and His G 46(6837) are presented. In toxicity studies exposure of human lymphocyte cultures to 1.3 X 10(-9) to 1.6 X 10(-5) M Se yielded sister chromatid exchange (SCE) rates equivalent to background levels of 6--7 SCE per cell. The SCE frequencies of lymphocytes cultured with Se and selected carcinogens are discussed.
TL;DR: It is found that S-adenosylmethionine levels remained depressed beyond the time when dimethyl selenide synthesis ceased, suggesting that selenite inactivated methionine adenosyltransferase.
TL;DR: Investigations of the possible anticancer value of selenium as well as its reported value against other chronic diseases should be made.
Abstract: The role of methylation of selenium in the aquatic environment adds to the knowledge of the selenium cycle in nature. Selenium deficiency is thought to represent far more of a problem than are any likely excesses of Se in the environment. Selenium should be viewed as an essential nutrient. Investigations of the possible anticancer value of selenium as well as its reported value against other chronic diseases should be made.
TL;DR: Selenium(VI) and total selenium in NBS Bovine Liver, SRM 1577, were determined successfully and 4,6-dibromopiazselenol, formed by the reaction of 1,2-diamino-3,5- dibromobenzene with selenous acid, was found to be best as regards sensitivity and distribution ratio.
TL;DR: A method is described for the routine determination of selenium in blood and plant samples at concentrations in the range 0.01–0.50 µg g–1 and the efficiency of hydride generation was 95%.
Abstract: A method is described for the routine determination of selenium in blood and plant samples at concentrations in the range 0.01–0.50 µg g–1. Samples of mass 1 g are digested with nitric and perchloric acids and then selenium hydride is generated from diluted digests by the controlled introduction of a solution of sodium borohydride. The selenium is subsequently atomised in a nitrogen-hydrogen-entrained air flame. Digests can be analysed at a rate of four per minute. For a pasture sample, which contained a 0.038 µg g–1 concentration of selenium, and a blood sample, which contained 0.029 µg g–1 of selenium, relative standard deviations of 7.9 and 4.3%, respectively, were obtained. The mean recovery of added selenium was 100.5%, with a relative standard deviation of 4.7%. The efficiency of hydride generation was 95%.