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PubMed2003

The chemical form of selenium affects insulinomimetic properties of the trace element: investigations in type II diabetic dbdb mice.

The objective of the present study was to investigate the effects of oral selenate application in comparison to selenium deficiency and selenite treatment on the development of the diabetic status (glucose tolerance, insulin resistance and activities of glycolytic and gluconeogenic marker enzymes) in dbdb mice, representing a type II diabetic animal model. Therefore 21 adult male dbdb mice were assigned to 3 experimental groups of 7 animals each and put on a selenium deficient diet (< 0.03 mg/kg diet) based on torula yeast. Group 0Se was kept on selenium deficiency for 10 weeks while the mice of the groups SeIV and SeVI were supplemented daily with 15% of their individual LD(50) of sodium selenite or sodium selenate in addition to the diet. After 10 weeks a distinct melioration of the diabetic status indicated by a corrected glucose tolerance and a lowered insulin resistance was measured in selenate treated mice (group SeVI) in comparison to their selenium deficient and selenite treated companions and to their initial status. Activities of the glycolytic marker enzymes hexokinase, phosphofructokinase and pyruvate kinase were increased 1.7 to 3-fold in liver and/or adipose tissue by selenate treatment as compared to mice on selenium deficiency and mice with selenite administration. In contrast selenate treatment (SeVI) repressed the activity of liver pyruvate carboxylase the first enzyme in gluconeogenesis by about 33% in comparison to the selenium deficient (0Se) and selenite treated mice (SeIV). However the current study revealed an insulinomimetic role for selenate (selenium VI) also in type II diabetic animals due to a melioration of insulin resistance. In contrast selenium deficiency and especially selenite (selenium IV) impaired the diabetic status of dbdb mice, demonstrating the need for investigations on the insulinomimetic action of selenium due to the metabolism of different selenium compounds.

Adipose Tissue↗
PubMed2003

Forms and distribution of selenium at different depths and among particle size fractions of three Taiwan soils.

The bioavailability of selenium in soils for plants depends more on its forms than on its total concentration. The purpose of the present study was to examine the solid-phase forms of selenium at different depths of three soil series representing major farming soil groups in Taiwan as well as the amounts of selenium in sand, silt and clay fractions of the soils. The study was conducted by means of sequential extraction to obtain the amounts of selenium and the distribution of various solid-phase forms of selenium at different depths of Pinchen (121 degrees 11(')E, 24 degrees 55(')N), Toulun-Sheto (120 degrees 55(')E, 24 degrees 50(')N), and Chunliao (120 degrees 25(')E, 23 degrees 57(')N) soil series. The amounts of metal oxide-bound form of selenium in the three soil series were the largest, with those of Pinchen and Toulun-Sheto soil series exceeding 50% of the total amounts of selenium and that of Chunliao soil series maintained at 30-40%. In the Pinchen and Toulun-Sheto soil series, the amounts of selenium in clay fractions were the largest, with a significant difference between the clays with and without metal oxides and organic matter removed. The amounts of selenium remained high in silt and/or sand fractions of the Chunliao soil series with metal oxides and organic matter removed. Metal oxide and organic matter contents of the three soil series mainly affect the amounts of various solid-phase forms of selenium and their distribution in different depths and particle size fractions of the soils. This observation of selenium associated with soil constituents was in good agreement with the results of the adsorption of selenite and selenate by the three soil series.

Adsorption↗
PubMed2006

Bioavailability of selenium from the selenotrisulphide derivative of lipoic acid.

BACKGROUND/PURPOSE: Selenium is a required micronutrient in mammals, needed for the activity of enzymes that contain selenocysteine at their active site. Several isoenzymes of glutathione peroxidase and thioredoxin reductase contain selenocysteine and thus the nutritional status of selenium in tissues can have significant impact on the steady state level of reactive oxygen species. The aims of this study were to evaluate the bioavailability of selenium derived from the selenotrisulfide derivative of lipoic acid (LASe) and determine the ability of this compound to be absorbed into skin. METHODS: Bioavailability of selenium derived from LASe was determined using a keratinocyte cell model (HaCat). Efficiency of utilization of selenium was assessed by following the decrease in the incorporation of radiolabeled selenite (75Se) in the presence of increasing concentration of selenium compounds. Percutaneous absorption of LASe was measured by determining selenium levels in full thickness biopsy of skin using a Yorkshire pig model. RESULTS: LASe was efficiently absorbed topically into pig skin, a good model of human skin. In a keratinocyte cell line LASe was an efficient source of selenium for selenoprotein synthesis, demonstrating that LASe is a good candidate as a topical selenium micronutrient. Both L-selenomethionine and selenate were found to be poor sources of selenium for selenoprotein synthesis in the skin cell model and L-selenomethionine was poorly absorbed into pig skin. CONCLUSION: These results indicate that stable selenotrisulfides, such as LASe, are good candidates for testing as topical selenium supplements.

Administration, Cutaneous↗
PubMedDate not supplied

Speciation and bioavailability of selenium in yeast-based intervention agents used in cancer chemoprevention studies.

This study investigated the speciation and bioavailability of selenium in yeast-based intervention agents from multiple manufacturers from several time points. Sources of selenized yeast included Nutrition 21 (San Diego, CA), which supplied the Nutritional Prevention of Cancer (NPC) Trial from 1981-1996; Cypress Systems (Fresno, CA; 1997-1999); and Pharma Nord (Vejle, Denmark; 1999-2000), which supplied the Prevention of Cancer by Intervention by Selenium (PRECISE) Trial pilot studies. The low-molecular-selenium species were liberated from the samples by proteolytic hydrolysis followed by separation by ion exchange liquid chromatography and detection by inductively coupled plasma-mass spectrometry. The results for the NPC tablets showed that selenomethionine, together with 3 unidentified selenium compounds, were predominant in the sample hydrolysates. The relative amounts of the 4 selenium species varied (p < 0.05) among several of the 7 tablet batches used during the course of the NPC Trial. In comparison, 5 batches of more recently produced selenized yeasts, which were used as a source of selenium in the PRECISE and other trials, contained less of the unknown compounds and more selenomethionine at 54-60% of the total selenium in the yeasts. One batch of yeast, however (from 1985), which originated from the same producer as the yeast used in the NPC tablets, contained only 27% of selenium in the sample as selenomethionine. Human subjects receiving 200 microg selenium/day in the UK PRECISE Pilot Trial showed a higher concentration (p < 0.01) and higher increase from baseline in plasma selenium than did the same dosage used in the NPC Trial. Differences in intake, speciation, or bioavailability of selenium from the yeast-based supplements in the population groups studied may explain this. Furthermore, the selenium concentration in whole blood from the Danish PRECISE Pilot Trial was higher (p < 0.001) than that obtained with synthetic L-selenomethionine in a comparable group of Danes, both groups having been treated with 300 microg selenium/day.

Anticarcinogenic Agents↗
PubMed2000

Effects of selenium pretreatment on cisplatin-induced chromosome aberrations in wistar rats.

Selenium is an essential trace element and a potent anticancer agent. Extensive laboratory studies demonstrate that selenium is an effective chemopreventive agent in various sites in animals. The administration of selenium as a chemopreventive agent raises the question whether the antioxidant selenium, alone or in combination with other dietary antioxidants, could protect non-tumor cells from the clastogenic effect of cisplatin. Therefore, the present study was undertaken to investigate the modulatory effects of selenium, combined or not with vitamin C, on cisplatin-induced chromosomal aberrations in Wistar rat bone marrow cells. The animals were sacrificed 18, 24, or 72 h after cisplatin injection. The results obtained in Wistar rat bone marrow cells showed a slight nonsignificant reduction in the total number of chromosomal aberrations induced by cisplatin (5 mg/kg b.w.) observed in the animals that received a pretreatment with a single dose of selenium (2 mg/kg b.w.). The administration of two doses of selenium (1 mg/kg b.w.) also did not inhibit the chromosomal damage induced by cisplatin. In the present study, no protective response was obtained with either a single or double dose of selenium in rats treated with cisplatin. Furthermore, the combination between selenium+vitamin C was no more effective than vitamin C alone in the protection against damage caused by this antitumor drug. Further investigations, with other forms of selenium, are necessary to elucidate a possible protective role of selenium in clastogenicity induced by free radicals generated by antitumor drugs.

Animals↗
PubMed2003

Insulin-like and non-insulin-like selenium actions in 3T3-L1 adipocytes.

In insulin-sensitive 3T3-L1 adipocytes, selenium stimulates glucose transport and antilipolysis and these actions of selenium, like insulin actions, are sensitive to wortmanin, an inhibitor of phosphatidylinositol-3-kinase (PI3K). Selenium stimulates PI3K activity that is sustained up to 24 h. Selenium after 5-10 min increases tyrosine phosphorylation of selective cellular proteins, but after 24 h overall tyrosine phosphorylation is increased. Tyrosine phosphorylation of insulin receptor substrate 1 is detected when enriched by immunoprecipitation with anti-PI3K antibody. Selenium, however, does not stimulate insulin receptor tyrosine kinase activity. Selenium also increases phosphorylation of other insulin signaling proteins, including Akt and extracellular signal regulated kinases. Selenium-stimulated glucose transport is accompanied by increases in glucose transporter-1 content in the plasma membrane. These data are consistent with similar selenium action in glucose transport in 3T3-L1 fibroblasts expressing mainly GLUT1. In chronic insulin-induced insulin resistant cells, selenium unlike insulin fully stimulates glucose transport. In summary, selenium stimulates glucose transport and antilipolysis in a PI3K-dependent manner, but independent of insulin receptor activation. Selenium exerts both insulin-like and non-insulin-like actions in cells.

3T3 Cells↗
PubMed2001

Effects of methylmercury and organic acid mercurials on the disposition of exogenous selenium in rats.

Interaction of methylmercury (MM), an environmental and industrial toxicant, with selenium is well known but incompletely understood. Therefore, the effects of MM (10 micromol/kg i.v.) on the disposition of exogenous selenium were compared with those of other organic mercurials (merbromine, mercuribenzene sulfonic acid, and mercuribenzoic acid) in anesthetized bile duct-cannulated rats injected with sodium [(75)Se]selenite (10 micromol/kg i.v.). The mercurial organic acids (10 micromol/kg i.v.) differed strikingly from MM in their influence on selenium disposition. They promoted renal and hepatic accumulation as well as biliary excretion of selenium but decreased distribution to the muscle, testis, and brain as well as the pulmonary excretion of selenium. In contrast, MM altered selenium distribution in an opposite fashion: it diminished the biliary output of selenium and enhanced selenium exhalation. GC-MS analysis verified that this latter paradoxical effect resulted from increased exhalation of dimethyl selenide. Further studies indicated that the MM-induced increase in pulmonary excretion of dimethyl selenide cannot be due to a diminished conversion of this volatile selenium compound to trimethylselenonium ion (TMSe(+)), because MM influenced neither the urinary excretion nor the hepatic and renal concentration of TMSe(+) in selenite-injected rats. Compared to the selenite-exposed rats, the selenite plus MM-injected animals exhibited a significant rise in the hepatic level of S-adenosylmethionine (SAME), the endogenous methyl donor in selenium methylation, and the ratio of SAME to S-adenosylhomocysteine. Based on these and others' observations, it is hypothesized that MM may increase hepatic availability of SAME in selenite-dosed rats by counteracting selenite-induced inactivation of SAME synthetase, thereby facilitating SAME synthesis, and/or by acting as a methyl donor in formation of dimethyl selenide, thereby sparing SAME. In summary, the toxicologically and ecologically relevant interaction of MM and selenite is not mimicked by organic acid mercurials, possibly because it results in formation of lipophilic Hg- and Se-containing common compound(s) and because it also appears to involve methyl transfer from MM to selenium.

Animals↗
PubMed1993

Selenium and the risk of postmenopausal breast cancer in the DOM cohort.

Selenium has been claimed to have chemo-preventive properties. However, data showing that in humans selenium levels are already decreased prior to diagnosis of breast cancer were not available. Such information is mandatory before oral selenium supplementation in the primary prevention of (breast) cancer in humans is acceptable. This question of a 'preventive-potential' of selenium was evaluated in a case-control study nested in a cohort, because this design allows determination of the time-order of preceding selenium levels and subsequent cancer risk. The cohort consisted of 5577 women aged 55-70 years from the DOM project, a population based breast cancer screening program in the Netherlands. Instrumental Neutron Activation Analysis was used to measure the selenium content of toenail clippings. The 69 cases of breast cancer found during follow-up after screening. represent 'recent' tumours since all women had a negative screening mammogram 3-5 years previously. No decreased selenium levels, as measured in nail clippings from the big toes, could be detected in cases-to-be, either when compared to 4 age matched controls per case or when compared with a random control group drawn from the entire cohort. On the contrary, a tendency for slightly higher selenium levels among 'future' cancer cases was observed. As to the sensitivity of detecting differences in selenium by nail clippings, lower selenium could be detected in nails of current smokers. The smoking-related decrease in nail selenium level was of the same order as the differences between breast cancer cases and controls, but was independent of the breast cancer risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Selenium accumulation and elimination in mallards.

Selenium accumulation and loss were measured in adult mallards (Anas platyrhynchos) fed selenomethionine during two experiments. In Experiment 1, both sexes were fed a diet containing 10 ppm selenium for 6 weeks, followed by 6 weeks on untreated feed. Selenium accumulation in liver and muscle of females was described by C = A(1-e-bt). Concentrations of selenium were predicted to reach 95% of equilibrium faster in liver (7.8 days) than in muscle (81 days). The loss of selenium from liver and muscle of females was described by the exponential loss rate equation: C = Ae-bt, with half-times of 18.7 and 30.1 days, respectively. Males reached similar levels of selenium in liver and breast muscle as females and declined to similar levels once selenium treatment ended. In Experiment 2, females were fed increasing levels of selenium until some died. Survivors were switched to an untreated diet and selenium was measured in blood, liver, and breast muscle over 64 days. The same equation as in Experiment 1, C = Ae-bt, was used to describe the loss of selenium from blood and muscle. Half-times were 9.8 and 23.9 days, respectively. For liver, the equation C = A1e-b1t + A2e-b2t was used. Selenium initially decreased in liver by one-half in 3.3 days, with subsequent half-times of 3.9, 6.0, and 45.1 days.

Animals↗
PubMed1983

The selenium content of edible mushrooms in Finland.

In this investigation the selenium contents of 142 mushroom samples were determined. The majority of the samples were wild Finnish mushroom species generally used for human consumption. The selenium contents of some cultivated mushrooms were also determined. In all, the material analyzed consisted of 38 different mushroom species. Selenium concentrations were assayed after modified wet and dry ashing, by atomic-absorption spectrometry using the hydride technique and the standard-addition procedure. The reliability of the method was tested with certified standard reference materials. The results of analysis obtained indicate that selenium contents vary considerably between different mushroom species. Of the species investigated, by far the highest selenium contents were found in Boletus edulis (mean 17 mg/kg dry weight). Other mushrooms having considerable selenium contents included Macrolepiota (5.0 mg/kg), wild Agaricus spp. (2.7 mg/kg), Gasteromycetes (1.9 mg/kg), Lactarius torminosus (1.9 mg/kg) and Marasmius oreades (1.6 mg/kg). The contents in these mushrooms are sufficient to provide an amount of selenium that is nutritionally significant in relation to the total daily intake of selenium of the Finnish population. Other edible mushrooms generally used in Finnland, e.g. species belonging to Cantharellaceae, Russula, Boletaceae (other than B. edulis) and Lactarius (other than L. torminosus) contained only small amounts of selenium. The importance of these mushrooms as a source of selenium is therefore marginal. The selenium content of Lactarius torminosus decreased by an average of 32% during the blanching necessary before consumption of these mushrooms.

Basidiomycota↗
PubMed1985

Low blood selenium levels in alcoholics with and without advanced liver disease. Correlations with clinical and nutritional status.

Selenium deficiency has been implicated as a cause of hepatic injury, possibly from accentuated lipoperoxidation due to decreased activity of the selenoenzyme, glutathione peroxidase. Because of possible clinical and biochemical links between selenium and alcohol, we performed nutritional assessment and assayed red blood cell, plasma, and whole blood selenium by spectrofluorometry in 27 normals (group I), 30 asymptomatic alcoholics on admission to a detoxification unit, (group II) and 16 alcoholics with severe liver disease (group III). We found a mean (+/- SD) whole blood selenium of 0.109 micrograms/ml +/- 0.014 for group I vs 0.076 +/- 0.010 for group II (P less than 0.001), and 0.047 +/- 0.006 for group III (P less than 0.001 vs group I and II). For plasma, the mean (+/- SD) selenium was 0.095 micrograms/ml +/- 0.016 for group I versus 0.065 micrograms/ml +/- 0.012 in group II and 0.038 micrograms/ml +/- 0.007 in group III (All P less than 0.001). Calculated red blood selenium levels were also significantly reduced in alcoholics versus controls. Whole blood and plasma selenium correlated directly with serum albumin. For whole blood selenium versus albumin, r = 0.73 (P less than 0.01), and for plasma selenium versus albumin, r = 0.71 (P less than 0.01). A significant inverse correlation was noted between whole blood selenium and the height of the total serum bilirubin (r = -0.46), alkaline phosphatase (r = -0.50), and AST (r = -0.51) (P less than 0.01 for all). Among alcoholics admitted for detoxification, selenium was diminished despite the absence of severe malnutrition, as determined by standard nutrition assessment parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Effect of dietary selenium and vitamin E on the biomechanical properties of rabbit bones.

It is generally agreed that combined deficiency of selenium and vitamin E leads to several abnormalities including Kashin-Beck disease which is an endemic and chronic degenerative osteoarthrosis. The abnormalities can be reversed by the administration of various forms of selenium and vitamin E. The present study was designed to investigate the effects of dietary selenium and vitamin E on bone tissue and on the biomechanical properties of bone. Young rabbits of both sexes were fed with either a selenium- and vitamin E-adequate diet (control group), or a selenium- and vitamin E-deficient diet or a selenium-excess diet. The selenium-deficient diet resulted in a significant decrease in plasma selenium level and the selenium-excess diet resulted in a significant increase in the plasma selenium level with respect to the corresponding control values (p < 0.05). The diets did not affect the blood cell counts considerably but erythrocyte glutathione peroxidase activity increased (decreased) relatively when the plasma selenium level increased (decreased) (p < 0.05). The light microscopic investigations of the bone tissues of the two experimental groups indicate that the findings of the present work are compatible with osteomalacia. The biomechanical properties of the bones from the three groups were determined experimentally with bending tests. Both the Se- and vitamin E-deficient diet and the Se-excess diet decreased the biomechanical strength of the bones significantly while the bones belonging to the control group always had the largest modulus of elasticity (p < 0.05).

Animals↗
PubMedDate not supplied

Serum selenium levels in Slovak population.

Blood serum selenium levels were measured in 576 healthy middle aged adults (40-60 yr, 255 men and 321 women) residing in both urban and rural areas in four districts of Slovakia. Serum selenium was determined by electrothermal AAS. The mean (+/- SD) serum selenium concentration was 0.852 +/- 0.335 mumol/L, ranging from 0.219-2.30 mumol/L. A large proportion of the individuals (19.62%) exhibited serum selenium levels under 0.57 mumol/L (45 mumol/L). There was no significant correlation between serum selenium concentration and age, sex, and smoking status. There were significant differences between districts. The lowest mean (+/- SD) serum selenium was 0.664 +/- 0.269 mumol/L, the highest mean serum selenium (+/- SD) was 0.975 +/- 0.361 mumol/L. This differences could probably be attributed to the selenium content in the soil of the different areas, which would contribute to the average daily selenium intake. In comparison with serum selenium levels in other European countries, the concentrations of selenium in the Slovak population are relatively low.

Adult↗
PubMedDate not supplied

Cadmium-induced alterations in ocular trace elements. Influence of dietary selenium and copper.

The present report demonstrates, for the first time, that feeding rats 50 ppm cadmium for just 7 wk results in detectable levels of cadmium in the eye of rats. Furthermore, these ocular cadmium concentrations affect significant alterations in the levels of the essential trace elements selenium, calcium, iron, and copper in the eye. Rats were fed a low-selenium (less than 0.02 ppm selenium), high-copper basal diet (50 ppm copper) supplemented with 0, 0.1, and 0.5 ppm selenium. The animals were either untreated or treated with 50 ppm cadmium admixed with their feed. Cadmium treatment resulted in significant reductions (up to 50%) in ocular selenium. Furthermore, rats fed the basal diet and given 100 ppm cadmium via their feed for 6 wk exhibited a 69% reduction in the activity of the selenoenzyme, glutathione peroxidase, in the eye. Cadmium treatment also resulted in reductions of up to 50% in ocular calcium, irrespective of dietary selenium supplementation. Iron levels were increased by 30% in rats fed the low-selenium diet and decreased by as much as 40% in rats fed the selenium-supplemented diets, compared to animals fed identical levels of selenium without cadmium. Ocular copper levels were significantly increased only in rats fed the low-selenium diet and treated with cadmium. Ocular zinc levels were not significantly affected by dietary cadmium or selenium.

Animals↗
PubMed1990

Selenium and cardiovascular disease.

For humans, ecological and epidemiological results are reported that show a relationship between the serum selenium concentration and cardiovascular disease in populations where low serum selenium concentrations are found, e.g., in Eastern Finland. From clinical studies done in Germany (FRG and GDR), Finland, and Sweden, subnormal serum selenium and partially whole blood selenium concentrations are reported in patients with acute myocardial infarction. For patients with coronary arteriosclerosis, subnormal serum selenium concentrations are reported from the USA and Germany and subnormal whole blood selenium concentrations from Germany. Subnormal serum and subnormal whole blood selenium concentrations of patients with cardiomyopathy are reported from non Keshan disease affected areas in Germany, France, and China. In selenium deficiency, an accumulation of lipid peroxides in the heart may occur, especially under ischemic conditions and if ischemic tissue is reperfused. Lipid peroxides in the heart may damage the cell membrane and may lead to an impaired calcium transport with an uncontrolled calcium accumulation in the cell. This may result in an activation of phospholipids, and, in consequence, to an enhanced formation of arachidonic acid. An increased concentration of lipid peroxides owing to selenium deficiency may shift the prostaglandin synthesis from prostacyclin to thromboxane, causing enhanced blood pressure and platelet aggregability. From animal experiments, it is known that selenium protects against cardiotoxic elements, cardiotoxic xenobiotics, and viral infections that affect the heart. Selenium deficiency may also be a secondary factor in the causation of hypertension and myocardial ischemia.

Animals↗
PubMedDate not supplied

Abnormalities of blood selenium and glutathione peroxidase activity in patients with acquired immunodeficiency syndrome and aids-related complex.

Severe protein-calorie malnutrition is common in patients with AIDS and could contribute to the progressive deterioration characteristic of that disease. Selenium deficiency could also have a negative impact on immune function and other organ functions vital for recovery from infectious diseases. Therefore, to assess any role for selenium in AIDS we determined plasma and erythrocyte selenium levels and glutathione peroxidase activity in 13 patients with AIDS compared to 8 patients with AIDS-related complex (ARC) and 14 healthy controls. Plasma selenium levels were significantly reduced in AIDS patients compared to controls (p less than .0001) and to ARC (p less than .02). Erythrocyte selenium levels in both AIDS and ARC were also reduced compared to controls (p less than .02), but not to each other. Glutathione peroxidase activity in AIDS was 28.9 +/- 1.4 U/g Hb vs 38.4 +/- 6.9 in ARC (p = NS) and 52.3 +/- 1.7 in controls (p less than .0001 vs AIDS; p less than .02 vs ARC). When all groups were combined, there were significant correlations between total lymphocyte count and both plasma selenium (r = .53; p less than .002) and erythrocyte glutathione peroxidase activity (r = .65; p less than .0001). In addition, strong correlations were noted between plasma selenium and serum albumin (r = .68; p less than .0001), plasma selenium and glutathione peroxidase (r = .77; p less than .0001), and glutathione peroxidase and hematocrit (r = .66; p less than .0001). In AIDS or ARC, no correlations between selenium with disease duration or weight loss were present. We conclude that, in comparison to normals, patients manifesting infection with human immunodeficiency virus have evidence of selenium deficiency as determined by diminished plasma and erythrocyte levels and glutathione peroxidase activity. These abnormalities are most marked in patients with AIDS, but are also present in patients with AIDS-related complex. Selenium deficiency has important implications for the progression and pathogenesis of clinical disease in AIDS.

AIDS-Related Complex↗
PubMed1999

[Significance of selenium in intensive care medicine. Clinical studies of patients with SIRS/sepsis syndrome].

Selenium is an essential component of the intracellular antioxidant system as a structural component of the active center of the glutathione peroxidase enzymes. These selenoenzymes play a major role in protecting cells against peroxidation, especially lipid peroxidation and selenium seems to play a direct role in the regulation of inflammatory processes. In conditions of systemic inflammatory response or sepsis, patients are exposed to severe oxidative stress. These patients already have both, a decreased plasma selenium and glutathione peroxidase activity at admission to the ICU as has been shown in several studies. The degree of selenium deficiency is correlated with the severity of disease and the incidence of mortality. The reason for the low plasma selenium levels is unknown. Especially it would be of interest a) if the low plasma selenium is the consequence of the systemic inflammatory response with distribution of selenium in other compartments of the body, b) most important, whether the substitution of selenium might improve the outcome and decrease the mortality rate of these patients. In 2 independently performed intention-to-treat studies including patients with systemic inflammatory response syndrome or sepsis a beneficial effect of selenium supplementation on multiple organ function and outcome could already be demonstrated as well as a tendency of an improved mortality rate. A prospective analytical study clearly could demonstrate the inverse relationship between low plasma selenium and morbidity and mortality of patients with SIRS/sepsis. The results of these studies are so convincing, that we propose a randomized, prospective, double blind multicenter phase-III study including patients with systemic inflammatory response syndrome or sepsis to investigate, whether a high-dose selenium substitution in addition to the recommended treatment strategies for patients with sepsis improves outcome and mortality rate of these patients.

APACHE↗
PubMed1982

Absorption, distribution, half-life and possible routes of elimination of dietary selenium in juvenile rainbow trout (Salmo gairdneri).

1. The influence of different levels of dietary selenium on the metabolism of selenium in rainbow trout was studied using 75Se as an indicator. 2. Gastric absorption of selenium by the trout appeared to be very efficient. 3. Highest tissue concentrations of selenium were noted in the liver and kidney. 4. Blood did not concentrate selenium and the plasma was the major transport medium. 5. The liver and kidney appeared to be involved in selenium excretion based on high tissue concentrations and variations in half-lives with selenium loading. 6. The biological half-life of selenium in the tissues decreased with increased selenium loading except in the liver, which at toxic dietary selenium concentrations became longer, suggesting a rate-limiting metabolic transformation of selenium for excretion in this organ.

Animals↗