Showing papers on "Selenium published in 1983"

Protein-free culture medium

Abstract: A trace element mixture suitable for use in a protein-free tissue culture medium, which comprises water-soluble compounds selected from acids, bases, and salts containing copper, iron, zinc, manganese, silicon, molybdenum, vanadium, nickel, tin, aluminum, silver, barium, bromine, cadmium, cobalt, chromium, fluorine, germanium, iodine, rubidium, zirconium, or selenium, the compounds being devoid of any additional metals other than those present as positive ions selected from groups IA and IIA of the periodic table of elements, wherein the compounds produce a solution containing specified minimum concentrations of the listed elements when dissolved in an amount of water sufficient to produce a concentration for one of the elements equal to the corresponding minimum concentration of the one element while maintaining each remaining element at a concentration equal to or greater than the minimum concentration for the remaining element is disclosed along with cell culture media containing these trace elements and methods of culturing cells using these media.

Biochemistry of selenium.

Abstract: 1. Forms of Selenium.- 1.1 Low Molecular-Weight Compounds.- 1.1.1 Selenocysteine.- 1.1.2 Selenocystine.- 1.1.3 Selenohomocystine.- 1.1.4 Se-methylselenocysteine.- 1.1.5 Selenocystathionine.- 1.1.6 Selenomethionine.- 1.1.7 Se-methylselenomethionine.- 1.1.8 Dimethyl Selenide.- 1.1.9 Dimethyl Diselenide.- 1.1.10 Trimethyl Selenonium.- 1.1.11 Elemental Selenium.- 1.1.12 Selenotaurine.- 1.1.13 Selenocoenzyme A.- 1.1.14 Other Compounds.- 1.2 Macromolecular Forms of Selenium.- 1.2.1 Formate Dehydrogenase.- 1.2.2 Glycine Reductase.- 1.2.3 Nicotinic Acid Hydroxylase.- 1.2.4 Xanthine Hydrogenase.- 1.2.5 Thiolase.- 1.2.6 Glutathione Peroxidase.- 1.2.7 Miscellaneous Selenoproteins.- 1.2.8 Seleno-tRNA's.- 11.11 References.- 2. Selenium Deficiency Diseases in Animals.- 2.1 Introduction.- 2.2 Dietary Liver Necrosis and Factor 3.- 2.2.1 Discovery.- 2.2.2 Pathology.- 2.2.3 Biochemical Defect.- 2.2.4 Hepatosis Dietetica.- 2.3 Nutritional Muscular Dystrophy.- 2.3.1 Pathology.- 2.3.2 Prevention of NMD.- 2.4 Exudative Diathesis.- 2.5 Pancreatic Degeneration.- 2.6 Mulberry Heart Disease.- 2.7 Reproductive Problems.- 2.8 Myopathy of the Gizzard.- 2.9 Growth.- 2.10 Selenium-Responsive Unthriftiness of Sheep and Cattle.- 2.11 Periodontal Disease of Ewes.- 2.12 Encephalomalacia.- 11.11 References.- 3. Metabolism of Selenium.- 3.1 Absorption.- 3.2 Placental Transfer.- 3.3 Mechanism of the Antioxidant Action of Selenium.- 3.4 Effect of Paraquat.- 3.5 Effect on Cytochrome P-450.- 3.6 Selenium and Hepatic Heme Metabolism.- 11.11 References.- 4. Comparative Metabolism and Biochemistry of Selenium and Sulphur.- 4.1 Introduction.- 4.2 Comparative Metabolism of Selenium and Sulphur.- 4.2.1 Microorganisms.- 4.2.2 Plants.- 4.2.3 Animals.- 4.3 Comparative Biochemistry of Selenium and Sulphur.- 4.3.1 Selenopersulfide as an Electron Transfer Catalyst.- 4.3.2 Iron-Sulphur Proteins.- 4.3.3 Sulphur Salts and Selenium Toxicity in Animals.- 4.3.4 Other Selenium-Sulphur Interactions.- 11.11 References.- 5. Biological Interactions of Selenium with Other Substances.- 5.1 Cadmium.- 5.1.1 Pathological Effects.- 5.1.2 Cadmium-Zinc Interactions.- 5.1.3 Cadmium-Selenium Interactions.- 5.1.4 Effect on Drug Response.- 5.2 Arsenic.- 5.3 Copper.- 5.4 Silver.- 5.5 Cobalt.- 5.6 Manganese.- 5.7 Lead.- 5.8 Mercury.- 5.8.1 Inorganic and Organic Mercury.- 5.8.2 Tissue Distribution.- 5.8.3 Properties of the Mercury-Selenium Complex.- 5.8.4 Teratogenicity.- 5.9 Thallium.- 5.10 Tellurium.- 5.11 Vanadium.- 5.12 Bismuth.- 5.13 Other Substances.- 11.11 References.- 6. Environmental Occurrence of Selenium.- 6.1 Geochemistry of Selenium.- 6.2 Soil Selenium.- 6.3 Uptake and Concentration of Trace Elements in the Roots, Stems, and Leaves of Plants.- 6.4 Forage Selenium.- 6.5 Selenium in Water.- 6.6 Selenium in Food.- 6.7 Intakes and Recommended Daily Allowance in Humans.- 6.8 Regulations in Regard to Animal Diets.- 11.11 References.- 7. Toxicity of Selenium.- 7.1 Introduction.- 7.1.1 Acute Toxicity.- 7.1.2 Blind Staggers.- 7.1.3 Alkalai Disease.- 7.1.4 Toxicity in Rabbits.- 7.1.5 Toxicity in Hamsters.- 7.1.6 Toxicity in Sheep.- 7.1.7 Toxicity in Rats.- 7.1.8 Effect of Diet on Toxicity.- 7.1.9 Biochemical Lesions.- 7.1.10 LD50 of Various Selenium Compounds.- 7.2 Industrial Medical Aspects.- 7.2.1 Occupational Hazards.- 7.2.2 Permissible Limits for Selenium Exposure.- 7.2.3 Toxicity in Humans.- 11.11 References.- 8. Selenium in Health and Disease.- 8.1 Selenium and Cancer.- 8.1.1 Skin Cancer.- 8.1.2 Liver Cancer.- 8.1.3 Colon Cancer.- 8.1.4 Breast Cancer.- 8.1.5 Tracheal Cancer.- 8.1.6 Chemotherapeutic Effect of Selenium.- 8.1.7 Epidemiological Relationship.- 8.1.8 Selenium Blood Levels in Cancer Patients.- 8.1.9 Selenium as a Carcinogen.- 8.2 Selenium and Mutagenesis.- 8.2.1 Antimutagenicity.- 8.2.2 Mutagenicity.- 8.3 Selenium and Immunity.- 8.3.1 Effect of Selenium on Humoral Immunity.- 8.3.2 Cell-Mediated Immunity.- 8.3.3 Nonspecific Immune Effects of Selenium.- 8.4 Selenium and Dental Caries.- 8.5 The Anti-Inflammatory Properties of Selenium.- 8.6 Selenium and Heart Disease.- 8.6.1 Animals.- 8.6.2 Humans.- 8.7 Selenium and Aging.- 8.8 Cystic Fibrosis.- 8.9 Multiple Sclerosis.- 8.10 Cataracts.- 8.11 Other Diseases.- 8.12 Radioselenium as a Diagnostic Agent.- 11.11 References.- 9. Synthetic Forms of Selenium and Their Chemotherapeutic Uses.- 9.1 Anti-Infective Agents.- 9.1.1 Antibacterial.- 9.1.2 Antiviral.- 9.2 Antifungal Agents.- 9.3 Antiparasitic Agents.- 9.4 Compounds Affecting the Central Nervous System.- 9.4.1 Hypnotics.- 9.4.2 Analgesics and Local Anesthetics.- 9.4.3 Tranquilizing Drugs.- 9.5 Compounds that Affect the Autonomic Nervous System.- 9.6 Compounds that Affect the Circulatory System.- 9.7 Anti-Inflammatory Compounds.- 9.8 Antihistamines.- 9.9 Anticancer Agents.- 9.10 Antiradiation Agents.- 9.11 Steroids.- 9.12 Selenocoenzyme A.- 9.13 Selenium-Containing Carbohydrates.- 9.14 Seleno-Amino Acids.- 11.11 References.- 10. Analytical Methods of Selenium Determination.- 10.1 Introduction.- 10.2 Sample Preparation and Storage.- 10.3 Destructive Analysis.- 10.3.1 Ashing.- 10.3.2 Closed-System Combustion.- 10.3.3 Wet Digestion.- 10.3.4 Measurement of Selenium.- 10.4 Nondestructive Analysis.- 10.4.1 Neutron Activation Analysis.- 10.4.2 X-Ray Fluorescence Analysis.- 10.4.3 Proton-Induced X-Ray Emission.- References.

Distribution of selenium and glutathione peroxidase in the rat.

Abstract: The selenium content was determined in the adrenals, brain, erythrocytes, femur, hair, heart, kidneys, lungs, muscle, pancreas, plasma, spleen, testes, and thymus of rats, which had been fed a commercial rat diet containing 03 mg Se/kg diet In the plasma, the erythrocytes, and the soluble fraction of the tissues (with the exception of femur and hair) the activity of the glutathione peroxidase (GSH-Px) was measured, using both hydrogen peroxide and t-butyl hydroperoxide as substrates From the masses of the tissues and the values for the selenium content and the GSH-Px activity, the distribution of the element and the enzyme in the body was calculated For selenium the main pools were the muscle and the liver, and for the GSH-Px, the liver and the erythrocytes By comparing the selenium content and the GSH-Px activity the percentage of the tissue selenium, which was bound to the enzyme in the soluble tissue fraction, was estimated This percentage differed considerably from tissue to tissue, the highest value being found in the erythrocytes and the smallest in the testes According to this estimation the majority of the selenium in the rat is not contained in the GSH-Px but in other compounds

Synergistic effect of vitamin E and selenium in the chemoprevention of mammary carcinogenesis in rats.

Abstract: The present study showed that vitamin E, although ineffective by itself, was able to potentiate the ability of selenium to inhibit the development of mammary tumors induced by dimethylbenz(a)anthracene (DMBA) in rats. Animals were maintained on a high-polyunsaturated fat (20% corn oil) diet in order to increase the degree of oxidant stress; additional selenium and/or vitamin E were present at a concentration of 2.5 and 1000 mg/kg of diet, respectively. It should be noted that rats tolerated these levels of supplementation very well with no obvious undesirable effect. Furthermore, our results indicated that vitamin E facilitated the anticarcinogenic action of selenium only when it was present during the proliferative phase. We then proceeded to examine whether DMBA administration would lead to any persistent damage in tissue peroxidation or changes in activities of enzymes associated with peroxide metabolism. It was found that DMBA resulted in an acute but modest increase in lipid peroxidation at 24 hr after carcinogen treatment. This perturbation was only of a transient nature. By comparing the response in a target tissue (mammary fat pad) and a non-target tissue (liver), it can be inferred that DMBA may have a differential effect on the degree of oxidant stress. The antagonistic effect of selenium and vitamin E in suppressing lipid peroxidation was then evaluated. Several conclusions can be drawn regarding the antioxidant potency of these agents in conjunction with their efficacies in cancer prevention. First, although vitamin E is a more effective antioxidant than selenium, it is apparent that systemic suppression of lipid peroxidation by vitamin E subsequent to a carcinogenic insult is not sufficient to inhibit tumor formation. Vitamin E supplementation increases significantly the microsomal hydroperoxidase activity. At the present time, it is unclear what role, if any, this enzyme plays in the synergistic effect of vitamin E and selenium in the inhibition of tumorigenesis. Secondly, the anticarcinogenic action of high levels of selenium is not related to its biochemical function in the regulation of the selenium-dependent glutathione peroxidase. The explanation for this is that the enzyme is already operating at near maximal capacity under normal physiological conditions. Additional selenium will not further increase its activity, since the enzyme protein becomes the limiting factor. Finally, vitamin E may be able to provide a more favorable climate against oxidant stress, thereby potentiating the action of selenium via some other mechanism.

Platelet glutathione peroxidase activity as an index of selenium status in rats.

Abstract: Glutathione peroxidase activity in platelets increased stepwise in selenium-depleted rats that were repleted with graded levels of dietary sodium selenite. In a 3-phase depletion/repletion/depletion feeding study, glutathione peroxidase activity was similar in platelets and liver, which apparently contains the largest labile pool of selenium in the body. The activity of glutathione S-transferase (selenium-independent glutathione peroxidase) in platelets was low and was not affected by selenium deficiency, even though hepatic transferase was markedly elevated in selenium-deficient rats. Vitamin E deficiency did not affect activities of glutathione peroxidase or glutathione S-transferase in platelets or liver. Determination of glutathione peroxidase activity in platelets apparently is a promising technique for assessing selenium status and, possibly, for measuring selenium bioavailability.

Biological Activity of Selenium

Abstract: EFFECT OF SELENIUM ON GLUTATHIONE METABOLISM AND GLUTATHIONEDEPENDENT ENZyMES 54 Glutathione Peroxidase 54 Glutathione S-Transferase 56 Glutathione. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Recapitulation 57 EFFECT OF SELENIUM ON XENOBIOTIC METABOLISM 57 Cytochrome P450 . .. . . . . . . .. . . . . . . . . ......... 58 Other Xenobiotic-Metabolizing Enzymes 61 OTHER EFFECTS OF SELENIUM 61 Vitamin E 61 Mercury 62 Others 62 EFFECTS OF SELENIUM IN WHOLE ANIMALS 63 Pure Selenium Deficiency 63 Effects of Selenium Deficiency on Responses to Drugs and Other Chemicals ......... 63 Effects of Selenium Deficiency on Carcinogenesis 65 Effects of Selenium in Man ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 CONCLUSIONS .... . . . . ...... ..... . . .. . . . . ..... . . . . . .. . ....... . . .... . 67

Dietary selenium in humans toenails as an indicator

Abstract: Mounting laboratory and epidemiologic evidence suggests that selenium may be important in the etiology of both cancer and heart disease. We explored the use of hair and nails as indicators of selenium intake by measuring their selenium levels using neutron activation analysis, a highly sensitive and precise nondestructive technique. Levels in duplicate samples of nails, hair, and blood were all reasonably reproducible. However, selenium-containing shampoos severely contaminated some of the hair specimens, suggesting that use of hair in epidemiologic studies could be misleading. The mean selenium level in toenails from South Dakota (a known high selenium area) was 1.17 ppm (1SE = 0.09). This was significantly higher than mean levels from Boston and Georgia (medium selenium intake area) of 0.74 ppm (0.04) and 0.81 (0.03), respectively. The mean selenium level in toenails from New Zealand (low selenium area) was 0.26 (0.02) and these levels did not overlap those of other areas. The South Dakota specimens showed marked familial aggregation, probably reflecting dietary differences. Since toenails vary in length, clippings from different toes represent different time periods of formation; clippings from all ten toes reflect selenium levels integrated over an extended period. As toenails are easily collected, transported, and stored, and reflect longterm intake, they can be useful in epidemiologic studies of selenium and chronic disease.

Effect of increased dietary carbohydrate on selenium metabolism and toxicity in rainbow trout (Salmo gairdneri).

Abstract: Juvenile trout were reared on either a high available carbohydrate (HC) or low available carbohydrate (LC) diet supplemented with from 0 to 10 micrograms selenium per gram of diet for 16 weeks, to determine if excess liver glycogen deposition affected the metabolism and toxicity of dietary selenium. Trout reared on the HC diet with 10 micrograms selenium per gram diet first demonstrated signs of selenosis and had significantly higher (P less than 0.05) liver selenium levels than trout reared on the LC diet with 10 micrograms selenium per gram diet after 16 weeks, indicating that excess dietary carbohydrate enhances dietary selenium toxicity in trout. The mechanism of the interaction is unclear since neither selenium elimination rates nor carcass and kidney selenium levels were affected by the dietary carbohydrate level. Trout reared on high dietary selenium diets (10 micrograms/g) had an increased incidence of renal calcinosis. In addition, liver copper levels were significantly affected by both dietary selenium and liver glycogen content indicating a significant copper-selenium and copper-glycogen interaction in trout. The development of renal calcinosis and the copper interactions suggest a variety of toxic effects of selenium on trout that may all be responsible for the observed changes in growth and feed efficiency.

The English ― Wabigoon river system. III: Selenium in lake enclosures: its geochemistry, bioaccumulation, and ability to reduce mercury bioaccumulation

Abstract: Aquatic biota have been shown previously to bioaccumulate selenium rapidly with a concomitant reduction in accumulation of mercury when exposed to 100 μg Se/L. Using radioisotope techniques this experiment extends these observations by examining the effects of single additions of sodium selenite at 1, 10, and 100 μg Se/L to experimental ecosystems (130 m3) located in mercury-contaminated Clay Lake, northwestern Ontario (50°03′N, 90°30′W). The major sink for added selenium and mercury was the sediment. Movement of 75Se into the sediments in control enclosures (< 0.2 μg Se/L) appeared to stabilize within 6 wk; however, movement did not stabilize in the selenium enclosures where selenium remaining in water was largely ionic. At first, selenium accumulated rapidly in net plankton but then declined in correspondence with water concentrations. In Anadonta sp. and Orconectes virilis, selenium increased with time and in proportion to ambient selenium. Stable concentrations of selenium were not achieved in fish af...

Serum selenium concentration related to myocardial infarction and fatty acid content of serum lipids.

Abstract: A longitudinal case-control study of 33 patients with one or more risk factors for coronary heart disease and 64 controls showed that the serum selenium concentration (range 0.63-1.33 mumol/l (50-105 micrograms/l] was not associated with development of clinical manifestations of coronary heart disease during a follow up of five to seven years. The content of polyunsaturated fatty acids, especially eicosapentaenoic acid, in serum cholesterol esters and phospholipids was positively correlated with selenium concentration. As a low content of polyunsaturated fatty acids in serum lipids was an independent risk factor for coronary heart disease in these subjects it may be hypothesised that the high coronary risk in subjects with a very low serum selenium concentration (less than 0.57 mumol/l (less than 45 micrograms/l] might be due not to selenium deficiency but to the coexisting low concentrations of polyunsaturated fatty acids in serum.

Determination of selenium in biological materials with platform furnace atomic-absorption spectroscopy and Zeeman background correction

Abstract: The presence of phosphate and iron provides a spectral interference for the determination of selenium at its primary resonance line at 196.0 nm that is avoided by using Zeeman background correction. Good quality pyrolytic graphite tubes, platform atomisation and integrated absorbance readings provide an acceptable quantitative environment for selenium and permit most analyses to be performed against a simple calibration graph using selenium in a nickel matrix modifier. Remaining problems appear to relate to loss of selenium prior to atomisation in the presence of certain matrices, notably the combination of sodium and sulphate. Charring in the presence of oxygen did not improve the analytical situation, nor did the use of silver, molybdenum or copper as a matrix modifier. We found a 2σ detection limit of 28 pg and a sensitivity of about 25 pg per 0.0044 As (A = absorbance units), expressed as characteristic amount. A preliminary direct method is presented for selenium in urine, with nickel, nitric acid and magnesium nitrate present, with a detection limit in urine of about 10 µg 1–1.

Electrothermal atomic absorption spectrometric determination of selenium in foods and diets.

Abstract: The validity of 2 electrothermal atomic absorption spectrometric methods for determination of selenium in foods and diets was tested. By using 0.5% Ni(II) as a matrix modifier to prevent selenium losses during the ashing step, it was shown that selenium can be determined in samples containing greater than or equal to 1 microgram Se/g dry wt without organic extraction. The mean recovery tested, using NBS Bovine Liver, was 98%; recovery of added inorganic selenium in Bovine Liver matrix was 100%. In addition, this method gave values closest to the median value of all participating laboratories using hydride generation AAS or the spectrofluorometric method in a collaborative study on high selenium wheat, flour, and toast samples. For samples with concentrations less than 1 microgram Se/g dry wt, separation of selenium from interfering Fe and P ions by organic extraction was necessary. Using inorganic 75Se in meat and human milk matrixes, an ammonium pyrrolidine dithiocarbamate-methyl isobutyl ketone-extraction system with added Cu(II) as a matrix modifier yielded the best extraction recoveries, 97 and 98%, respectively. Accuracy and precision of the method were tested using several official and unofficial biological standard materials. The mean accuracy was within 4% of the certified or best values of the standard materials and the day-to-day variation was 9%. The Se/Fe or Se/P interference limits proved to be low enough not to affect selenium determinations in practically all foods or diets. The practical detection limit of the method was 3 ng Se/g dry wt for 1.0 g dry wt samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors influencing the antitumorigenic properties of selenium in mice.

Abstract: Sodium selenite (Na2SeO3) was administered at 2.0 micrograms selenium (Se) to Swiss ICR mice six times over a 9-day period by intraperitoneal (i.p.) injection or by gastric gavage. Survival time was significantly increased in Ehrlich ascites tumor (EAT)-bearing mice by 170 and 20%, respectively, compared to controls. In two separate studies, 5.0 micrograms Se as Na2SeO3 or selenodiglutathione (GSSeSG) administered i.p. was more effective in inhibiting EAT propagation in mice than either untreated (control) mice or mice receiving sodium selenide, dimethyl selenide [(CH3)2Se] or seleno-DL-cystine. In another study, EAT cells were preincubated with either 1 or 3 ppm Se as GSSeSG, Na2SeO3, or (CH3)2Se, washed, and reinoculated into mice. Only in mice inoculated with cells pretreated with GSSeSG was a significant increase in survival observed. The observed tumor inhibition was not limited to ascitic tumors since growth of solid Ehrlich tumors was also significantly inhibited by i.p. treatment of Na2SeO3. Following i.p. administration of Na2(75)SeO3, the solid tumors retained more selenium-75 than did blood, lung, kidney, or liver. Supplementation of a torula yeast diet with 2.5 or 5.0 ppm Se as Na2SeO3 also significantly increased the survival time of EAT-bearing mice. These data show that the form and mode of administration of selenium influence the antitumorigenic properties of this trace element. In addition, the data suggest that some intermediate in the normal pathway for selenium detoxification is probably responsible for this trace element's antitumorigenic properties.

The selenium status of Belgian population groups : II. Newborns, children, and the aged.

Abstract: The selenium state of 40 elderly Belgian people, residing in geriatric homes, has been evaluated. Data are presented on the selenium (Se) contents of their blood, plasma, and erythrocytes. The activity of glutathione peroxidase (GSH-Px) has been assayed. All data were compared with those obtained for 164 young, working adults as presented in Part I of this study. Plasma selenium levels were significantly lower in the old (73 ng/mL) as compared to the young people (97 ng/mL), but erythrocyte Se levels (200 ng/mL) and GSH-Px activity were significantly higher. The selenium concentration in plasma during infancy has also been estimated. The results reveal a very low Se level during the first months of life, with a gradual increase with age. The results are discussed in the light of literature data.

Distribution of selenium and glutathione peroxidase in blood fractions from humans, rhesus and squirrel monkeys, rats and sheep.

Abstract: The distribution of selenium and glutathione peroxidase (GSH-Px) was investigated in blood fractions from humans, rhesus and squirrel monkeys, sheep and rats by gel filtration (Sephadex G-150). The majority of selenium in plasma and erythrocytes from sheep, squirrel monkeys and rats cochromatographed with GSH-Px. In contrast, selenium in plasma from humans and rhesus monkeys cochromatographed with two non-GSH-Px proteins and nearly all of the selenium in erythrocytes cochromatographed with the hemoglobin peak. A significant amount of GSH-Px activity in rhesus monkey and human erythrocytes also cochromatographed with the hemoglobin fraction, but very little GSH-Px coeluted with hemoglobin from squirrel monkeys, ovine and rat blood. The results suggest that GSH-Px activity may not be a good measure of selenium status in higher primates.

Selenium and immune functions in humans.

Abstract: Earlier animal experiments have shown that selenium depletion may decrease immune functions. In this human study, 40 volunteers from a population with low serum selenium concentrations were supplemented with selenium or placebo for 11 weeks. Blood samples were drawn at intervals for analysis of selenium status and immune function. At the end of the supplementation period, plasma selenium levels were 74 ng/ml in the placebo group and 169 ng/ml in the supplemented group. The improvement in selenium status was associated with a 57% increase in the activity of platelet glutathione peroxidase in the group supplemented with selenium, but there was no increase in the activity of this enzyme in the placebo-treated subjects. Immune function was measured in vitro by tests of lymphocyte and granulocyte activity. Intracellular killing of Staphylococcus aureus by granulocytes was slightly lower in the placebo group than in the selenium group at the end of the supplementation period (77.2 compared to 85.2%; P less than 0.05). No significant changes were observed in phagocytosis, chemotactic factor generation, antibody or leukocyte migration inhibitory factor production by lymphocytes, or proliferative responses to phytohemagglutinin or concanavalin A. These results suggest that the selenium deficiency of the order found in Finland and some other areas of the world has little, if any, influence on the immune functions measured in this study.

Considerations in the design of selenium bioavailability studies.

Abstract: Recommendations for safe and adequate dietary intakes of selenium were recently established. The recommendations were based largely on data from animals, because few data for humans were available. Some information regarding the dietary selenium intake required by humans to replace excretory losses has now appeared, but the bioavailability to humans of selenium from different dietary sources has not been determined. Selenium bioavailability depends on several metabolic processes, including not only absorption but also conversion into a biochemically active form. Of the different forms of selenium in foods, probably not all are converted to biologically active selenium with equal ease. Therefore, determination of selenium absorption may not in itself yield an accurate estimate of selenium bioavailability. Rather, functional tests, such as measurement of the selenoenzyme glutathione peroxidase, apparently are more valid for determining selenium bioavailability. Various food sources of selenium for humans differ widely in their ability to restore hepatic glutathione peroxidase activity in selenium-depleted rats. Platelet glutathione peroxidase activity seems to be particularly promising for bioavailability studies because platelets are a convenient biopsy material and the platelet enzyme is sensitive to changes in dietary selenium intake. Work in progress should establish the feasibility of this approach for future research in this area.