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PubMed1992

Selenium status of Christchurch infants and the effect of diet.

OBJECT: New Zealanders, because of a soil deficiency, have a low intake of selenium. To determine the impact of this on the infant population in Christchurch. METHODS: we have measured red cell and plasma selenium and the selenoenzyme, glutathione peroxidase, in 70 infants less than 12 months old and related these to age and diet. RESULTS: the infant population as a whole had mean plasma levels of selenium and glutathione peroxidase of 33 micrograms/L and 97 U/L compared with adult values of 74 micrograms/L and 150 U/L. Infant red cell levels of 0.30 mu g selenium and 9.0 U glutathione peroxidase per g haemoglobin were similar to those in adults. The selenium status of most breast fed infants after birth remained similar to that of cord blood. Mean plasma selenium and glutathione peroxidase levels in formula fed infants were about half those of breast fed infants, and their red cell selenium was also significantly lower. These did not increase until solids were introduced into the diet. The status of the infants reflected their diet, with the concentration of selenium in formulae being 3.9-5.2 micrograms/mL compared with a mean of 13.4 micrograms/mL in breast milk. CONCLUSIONS: since infants in more replete selenium areas show a gradual rise in blood selenium parameters after birth, this study suggests that formula fed and some breast fed infants in Christchurch receive an inadequate selenium intake. Consideration should be given to supplementing infant formulae and perhaps also the diet of pregnant and/or breast feeding mothers.

Adult↗
PubMed2003

Serum selenium levels in alcoholic liver disease.

BACKGROUND: The pathomechanism of liver damage in chronic alcoholic liver disease has not been fully elucidated yet. It seems undoubted that one of the mechanisms of alcohol-induced liver damage involves free radical reactions leading to peroxidation of proteins and lipids. The most important defense mechanisms are associated with the activity of antioxidative enzymes, among which glutathione peroxidase (GSH-Px), belonging to so-called 'free radical scavengers' should be mentioned. Selenium, regarded as a bioelement, is present in GSH-Px. Involved in numerous redox reactions, it belongs to the factors protecting the organism from oxidative shock. The aim of the study was to determine the selenium levels in blood serum of chronic alcohol abusers and to find potential correlations with the parameters of liver damage. MATERIAL/METHODS: The study was carried out in a group of 25 subjects (21 males, 4 females), treated in the Clinic or Outpatient Department of Hepatology for chronic alcoholic liver disease. At the time of the study, the patients had abstained from drinking for a period from one month to a year. Selenium was determined with atomic absorption spectroscopy method, using the hydride generation technique. The control group consisted of 11 males and 7 females. RESULTS: Statistical analyses of the control group indicated a significantly higher blood serum selenium level in males than in females. The patients demonstrated elevated aminotransferase activity, normal Falk, markedly increased GGTP. Mean INR was 1.4 and albumin concentration 3.3 g/l. Blood serum selenium levels in male patients were significantly lower in comparison with normal values. The analysis of correlations between some liver function parameters and selenium levels demonstrated a positive correlation between the levels of albumin and selenium. Serum selenium level was inversely proportional to ALAT activity. No correlations between selenium levels and INR levels, or GGTP activity were found. CONCLUSIONS: 1. Serum selenium levels differ in male and female populations. In healthy men, the level of Se in the serum is higher. 2. Antioxidative activity measured by serum Se level is low in men with chronic alcoholic liver disease (during the abstinence period). 3. Increased selenium level in the hair may indicate the presence of certain antioxidative reserve, which requires further studies.

Case-Control Studies↗
PubMed1990

The induction of specific rat liver glutathione S-transferase subunits under inadequate selenium nutrition causes an increase in prostaglandin F2 alpha formation.

We have reported previously that a dietary deficiency in selenium results in an increase in glutathione S-transferase (GST) activity of various rat tissues. In order to verify that the increased GST activity observed in a selenium deficiency results from increased synthesis of GST protein, cytosolic fractions of livers obtained from rats fed selenium-deficient and selenium-supplemented diets were analyzed by Western (protein) blots. Antisera raised against purified individual GST subunits (Ya, Yb, and Yc) were used to detect the corresponding subunits on the blots. The Ya subunit was induced 2.5-fold in the selenium-deficient state. The amount of Yc subunit also increased significantly (p less than 0.05) in selenium deficiency but not to the extent of the Ya subunit. The Yb subunit was not significantly affected by altered selenium nutritional status. A corresponding increase in poly(A) RNAs coding for the Ya and Yc subunits was also observed by Northern blot analysis. Transcriptional activity of GST YaYc genes was elevated by approximately 2-fold in purified nuclei isolated from selenium-deficient rat livers, which is sufficient to account for the increase in YaYc mRNA levels. Therefore, it appears that transcriptional activation of rat liver YaYc genes is the primary cause for the elevation of the corresponding gene products in the selenium-deficient state. Since the GSTs, especially the isozymes containing Ya subunit, have been implicated in the formation of prostaglandin (PG) F2 alpha, we investigated the effect of selenium deficiency on the PGF2 alpha-forming activity using a specific inhibitor of GSTs, S-decyl-GSH. In rats fed a nutritionally adequate diet, the activity inhibited by S-decyl-GSH accounted for at least half of the conversion of PGH2 to PGF2 alpha. During selenium deficiency, this GST-catalyzed activity was approximately doubled with no change in PGF2 alpha formation by other pathways, resulting in a 2-fold increase in overall synthesis of PGF2 alpha. These data strongly support a role of GSTs, especially those composed of the Ya size subunit, in the synthesis of PGF2 alpha from PGH2.

Animals↗
PubMed1991

Chemical form of selenium, critical metabolites, and cancer prevention.

Methylated selenides are prominent metabolites at the dietary levels used for obtaining anticarcinogenic effects with selenium. The present study reports the chemopreventive activities of 2 novel selenium compounds, Se-methylselenocysteine and dimethyl selenoxide, in the rat dimethylbenz(a)anthracene-induced mammary tumor model. Other treatment groups were supplemented with either selenite or selenocystine for comparative purposes. Each selenium compound was tested at different levels and was given to the animal starting 1 week before dimethylbenz(a)anthracene administration and continued until sacrifice. Results of the carcinogenesis experiments showed that the relative efficacy with the four compounds was Se-methylselenocysteine greater than selenite greater than selenocystine greater than dimethyl selenoxide. In correlating the chemical form and metabolism of these selenium compounds with their anticarcinogenic activity, it is concluded that: (a) selenium compounds that are able to generate a steady stream of methylated metabolites, particularly the monomethylated species, are likely to have good chemopreventive potential; (b) anticarcinogenic activity is lower for selenoamino acids, such as selenocysteine following conversion from selenocystine, which have an escape mechanism via random, nonstoichiometric incorporation into proteins; and (c) forms of selenium, as exemplified by dimethyl selenoxide, which are metabolized rapidly and quantitatively to dimethyl selenide and trimethylselenonium and excreted, are likely to be poor choices. We also undertook a separate bioavailability study using Se-methylselenocysteine, dimethyl selenoxide, and trimethylselenonium as the starting compounds for delivering selenium with one, two, or three methyl groups, and measured the ability of these compounds to restore glutathione peroxidase activity in selenium-depleted animals. All three compounds were able to fully replete this enzyme, although with a wide range of efficiency (Se-methylselenocysteine greater than dimethyl selenoxide greater than trimethylselenonium), suggesting that complete demethylation to inorganic selenium is a normal process of selenium metabolism. However, the degree to which this occurs under chemoprevention conditions would argue against the involvement of selenoproteins in the anticarcinogenic action of these selenium compounds.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Human selenium status and glutathione peroxidase activity in north-west England.

Nutritional selenium deficiency disease, due to low soil selenium content, is well recognized in British livestock. The adequacy of the selenium status of 25 healthy human volunteers, 50 blood donors, 94 general medical patients and 106 allergy clinic patients was investigated in 1987/8 by measuring serum selenium concentration and platelet glutathione peroxidase activity. Mean serum selenium concentration for the entire study population was 92 micrograms/l. Significant linear correlations between serum selenium concentration and peroxidase activity indicate that a substantial proportion of both healthy volunteers and medical patients are of low selenium nutritional status. Twenty-five per cent of healthy volunteers and 50 per cent of medical patients had serum selenium values below those required for full expression of selenium-dependent enzyme activity. Deficiency of the antioxidant activities of selenium and selenium-dependent enzymes may be relevant to geographical differences in morbidity from a wide range of human disease states.

Administration, Oral↗
PubMed1985

Incorporation and distribution of selenium into thiolase from Clostridium kluyveri.

Clostridium kluyveri incorporates selenium as selenomethionine into its acetoacetyl-CoA thiolase when grown in media containing normal sulfur-to-selenium ratios. Antibodies raised against the purified enzyme permitted quantitative immunoprecipitation of thiolase from crude cell extracts and thus facilitated the systematic analysis of the effects of wide variation in sulfur-to-selenium ratios on selenium incorporation into the enzyme. The extent of incorporation of selenium into thiolase was found to be dependent on the form of selenium supplied. When [75Se]selenomethionine was the source of selenium, the incorporation of selenium into thiolase was inversely proportional to the level of added methionine. However, similar levels of methionine failed to decrease the incorporation of selenium from selenite. To study the location of selenomethionine and methionine residues in the polypeptide chain of the enzyme, thiolase was prepared from cells cultured in the presence of H2 35SO4 or Na2 75SeO3. The 35S- or 75Se-labeled protein was treated with trypsin and the resulting peptides were isolated by reverse phase high performance liquid chromatography. The peptide maps of the enzyme indicated that selenium was distributed throughout the primary structure in a manner that paralleled methionine. From these studies, it is concluded that selenium occurs in thiolase adventitiously and is not required for any biological function.

Acetyl-CoA C-Acetyltransferase↗
PubMed1988

Serum selenium concentration in maternal and umbilical cord blood. Relation to course and outcome of pregnancy.

The present knowledge of the role of selenium in human fetal and neonatal development is sparse. In this study we measured serum selenium concentrations in maternal and umbilical cord blood from 500 Danish mothers at delivery, looking for a relationship between various maternal and fetal complications and selenium values. In mothers with uncomplicated pregnancies and deliveries serum selenium concentrations were 0.84 +/- 0.19 mumol/l (mean +/- SD), whereas in cord blood from full-term babies born adequate for gestational age and with no malformations serum selenium concentrations were 0.60 +/- 0.11 mumol/l (mean +/- SD). Mothers who received mineral tablets (other than iron preparations) during pregnancy had significantly higher serum selenium values than unsupplemented mothers (0.92 versus 0.70 mumol/l) (p less than 0.001). Infants of mineral-supplemented mothers also had significantly higher serum selenium values than infants of unsupplemented mothers (0.62 versus 0.58 mumol/l) (p less than 0.001). Preterm infants had significantly lower serum selenium concentrations than full term infants (0.54 versus 0.60 mumol/l) (p = 0.01), whereas infants small for gestational age did not differ in serum selenium concentrations from infants adequate for gestational age. Serum selenium concentrations in malformed infants tended to be lower than in normal infants (0.55 versus 0.60 mumol/l) (p = 0.09), but the difference was not statistically significant, probably due to the small number. Serum selenium concentrations in mothers with various complications during pregnancy and delivery did not differ from values in mothers with uncomplicated pregnancies and deliveries.

Adolescent↗
PubMed1987

Differential effects of dietary selenium on hepatic and renal glutathione-related enzymes and on hepatic microsomal drug metabolism in the rat.

These studies were undertaken to assess the effect of dietary selenium on glutathione-related enzyme activities in the liver and kidney and on hepatic drug metabolism. The intent was to study underlying mechanisms of selenium-induced beneficial effects in some models of hepatoxicity and carcinogenesis. Dietary selenium, as sodium selenite, was incorporated into a torula yeast basal diet (0.02 ppm selenium) and fed to male rats at supplementation levels of 0.0-5.0 ppm selenium for periods of three or six weeks. Additionally, a commercial cereal-based diet (CD, 0.05-0.08 ppm selenium) was compared to the experimentally defined diet (DD) supplemented with approximately the same amount of selenium. Liver and kidney glutathione peroxidase activity essentially plateaued at levels of selenium of 0.1 ppm and greater. CD- and DD-fed animals had hepatic and renal glutathione peroxidase activities which were similar. Glutathione S-transferase activity in liver, but not kidney, increased with increasing supplements of selenium. Glutathione S-transferase activities in CD- and DD-fed rats were not different. Cytochrome P-450 content and associated oxidative drug metabolism activities were relatively unmodified by selenium. Overall, dietary selenium appeared to act by enhancing potential conjugative detoxication pathway, rather than by decreasing the potential activation of chemicals via the hepatic cytochrome P-450 system.

Animals↗
PubMed1982

Effect of selenium deficiency and vitamin E deficiency on glutathione metabolism in isolated rat hepatocytes.

Selenium deficiency and vitamin E deficiency both affect xenobiotic metabolism and toxicity. In addition, selenium deficiency causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione metabolism in isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during the 5-h incubation. Freshly isolated hepatocytes had the same glutathione concentration regardless of diet group. During the incubation, however, the glutathione concentration in selenium-deficient hepatocytes rose to 1.4 times that in control hepatocytes. The selenium-deficient cells also released twice as much glutathione into the incubation medium as did the control cells. Total glutathione (intracellular plus extracellular) in the incubation flask increased from 47.7 +/- 8.9 to 152 +/- 16.5 nmol/10(6) selenium-deficient cells over 5 h compared with an increase from 46.7 +/- 7.1 to 92.0 +/- 17.4 nmol/10(6) control cells and from 47.7 +/- 11.7 to 79.5 +/- 24.9 nmol/10(6) vitamin E-deficient cells. This overall increase in glutathione concentration suggested that glutathione synthesis was accelerated by selenium deficiency. The activity of gamma-glutamylcysteine synthetase was twice as great in selenium-deficient liver supernatant (105,000 X g) as in vitamin E-deficient or control liver supernatant (105,000 X g). Hemoglobin-free perfused livers were used to determine the form of glutathione released and its route. Selenium-deficient livers released 4 times as much GSH into the caval perfusate as did control livers. Plasma glutathione concentration in selenium-deficient rats was found to be 2-fold that in control rats, suggesting that increased GSH synthesis and release is an in vivo phenomenon associated with selenium deficiency.

Animals↗
PubMed1980

Selenium and vitamin E in horses.

A survey of selenium and vitamin E concentrations in horses was conducted at four breeding farms in New York. There were no significant changes in mean blood selenium concentrations in horses at the three sampling dates whereas vitamin E concentrations underwent seasonal fluctuations. The mean blood selenium concentration in this survey for horses fed local feed was 7.7 microgram/dl. Horses fed commercial feed had a mean blood selenium concentration of 15.6 microgram/dl. A 0.94 correlation coefficient was found between blood glutatione peroxidase activity and blood selenium concentrations in horses. The effect of oral and parenteral selenium administration on blood selenium concentrations and blood glutathione peroxidase activity was also investigated. Oral supplementation of 1 mg selenium per day increased blood selenium concentrations above levels associated with myodegeneration in horses and foals. Parenteral supplementation trials with mares at late gestation indicate that only limited amounts of selenium cross the placental barrier. Parenteral supplementation of mares during gestation and lactation or supplementation of foals beginning at birth will increase blood selenium levels in foals above that associated with selenium/vitamin E deficiency.

Administration, Oral↗
PubMed1995

[Serum selenium levels in children and adolescents in selected regions in Slovakia].

BACKGROUND: There is a limited number of data concerning blood serum selenium levels in children and adolescents in the Slovak Republic. OBJECTIVES: The aim of this study was to access blood serum selenium levels in 102 healthy children (11-14 y) and 122 adolescents (15-18 y) from two regions: The district of Cadca and Modra--Pezinok area. METHODS: Serum selenium was determined by electrothermal atomic absorption spectrophotometric method using Pd as a matrix modifier. RESULTS: The mean (+/- SD) serum selenium concentration was 0.644 +/- 0.154 mumol/l in children and 0.730 +/- 0.175 mumol/l in adolescents. A large proportion of the individuals (28.43% in the children group, vs 14.05% in adolescent group) exhibited serum selenium levels below 0.57 mumol/l (45 micrograms/l). A significant correlation between serum selenium concentration and age (p < 0.001) was found. The correlation between serum selenium concentration and sex was not significant. CONCLUSIONS: In comparison with serum selenium levels in children and adolescents from other countries, the concentration of serum selenium in Slovak children and adolescents is relatively low. This differences could probably be attributed to the selenium content in the soil and to the lower average daily selenium intake via food. (Tab. 5, Fig. 2, Ref. 32).

Adolescent↗
PubMed1995

The relationship of selenium status to respiratory outcome in the very low birth weight infant.

OBJECTIVE: To examine the relationship between plasma and erythrocyte selenium and glutathione peroxidase (GPx) levels in premature infants and outcome measures. DESIGN: Prospective observational longitudinal study. SETTING: Two regional neonatal intensive care units in the South Island of New Zealand, an area with low soil selenium. PATIENTS: Seventy-nine infants with birth weights less than 1500 g or gestation less than 32 weeks admitted within 48 hours of birth from November 1992 through November 1993. MAIN OUTCOME MEASURES: Oxygen requirement at 28 days (chronic lung disease), or 36 weeks postmenstrual age and for all or most of the time from birth (bronchopulmonary dysplasia), total days in oxygen, retinopathy of prematurity, periventricular hemorrhage, or ventricular dilatation. RESULTS: Initial infant plasma selenium and GPx levels were about two thirds of maternal levels and fell a further 30% in 28 days. In contrast to adults, there was a poor correlation in infant plasma between selenium and GPx at birth and 28 days. Plasma selenium at 28 days was significantly lower in infants with chronic lung disease and bronchopulmonary dysplasia. After controlling for gestational age and age when fully fed orally, 28-day plasma selenium was significantly associated with the log of total days of oxygen requirement, each drop of 0.1 mumol/L in 28-day selenium being associated with a 58% increase in days of oxygen dependency. No significant associations of other parameters of selenium status and respiratory outcome were found, and there were no significant associations of any parameters of selenium status with other outcome measures. CONCLUSIONS: This study demonstrates for the first time in human infants that low plasma selenium levels are significantly associated with an increased respiratory morbidity. Whether selenium deficiency is etiologically important in determining the respiratory outcome or the result of sickness in the infant should be investigated in a randomized, controlled trial.

Bronchopulmonary Dysplasia↗
PubMed1995

Comparison of maternal blood and fetal liver selenium concentrations in cattle in California.

Selenium concentration was measured in paired maternal blood samples and fetal liver specimens collected at a San Joaquin County, Calif, slaughterhouse (beef = 19, dairy = 54) and from bovine aborted fetuses submitted to the California Veterinary Diagnostic Laboratory System (CVDLS; beef = 20, dairy = 20). Of the slaughterhouse samples and specimens, dairy maternal blood selenium concentration was significantly (P < 0.001) higher (mean +/- SD; 0.22 +/- 0.056 microgram/ml) than that for beef breeds (0.137 +/- 0.082 microgram/ml). The CVDLS mean maternal blood selenium concentration for the dairy-breed samples (0.192 +/- 0.028 microgram/ml) was similar to that for the slaughterhouse dairy-breed samples, but was greater than that for the slaughterhouse beef-breed samples. Slaughterhouse mean fetal liver selenium content also was higher (P < 0.001) for the dairy breeds (0.777 +/- 0.408 microgram/g), compared with the beef breeds (0.443 +/- 0.038 microgram/g). Mean fetal liver selenium content for slaughterhouse specimens was higher (P < 0.002) than that for the CVDLS specimens (beef, 0.244 +/- 0.149 microgram/g; dairy, 0.390 +/- 0.165 microgram/g). At the CVDLS, dairy fetal liver content was greater (P < 0.001) than that for beef breeds. Mean ratio of fetal liver selenium content to maternal blood selenium concentration was 3.53 +/- 1.89 for dairy breeds at the slaughterhouse (liver-to-blood correlation [r] = 0.38), and was 2.11 +/- 1.00 for dairy breeds at the CVDLS (r = 0.31) and 3.43 +/- 1.50 for beef breeds (r = 0.58). Both slaughterhouse breed ratios were significantly (P < 0.002) greater than the CVDLS dairy-breed ratio. On the basis of these results, breed and source location should be taken into account when interpreting selenium values. Fetal liver selenium content should only be used as a screening test and combined with whole blood selenium concentration from clinically normal herdmates to evaluate herd selenium status.

Abattoirs↗
PubMed2006

Selenium for alleviating the side effects of chemotherapy, radiotherapy and surgery in cancer patients.

BACKGROUND: Selenium supplements are frequently used by cancer patients. Selenium is an essential trace element and is involved in antioxidant protection and redox-regulation in humans. Several adverse effects of radiotherapy and chemotherapy in cancer patients as well as cellular processes that maintain chronic lymphoedema have been linked to oxidative cell damage in the human body. Selenium has recently been investigated as a remedy against chemotherapy and radiotherapy-associated side effects as well as its effects on lymphoedema. OBJECTIVES: This review assessed the effects of supplementary selenium on adverse effects of conventional radiotherapy, chemotherapy, or surgery, in oncologic patients and on quality of life or performance status during and after oncologic treatment. SEARCH STRATEGY: We searched the Cochrane Pain, Palliative & Supportive Care Trials Register, the Cochrane Database of Systematic Reviews (The Cochrane Library , Issue 2, 2004), Medline (1966 - Sep 2004), Embase (1980 - 2004 week 12), SIGLE (October 2004), Cancerlit (October 2004), Clinical Contents in Medicine CCMed (October 2004), the German Register of Cancer Studies (October 2004), the NCI Clinical Trials Register (October 2004), the International Standard Randomised Controlled Trial Number Register ISRCTN (October 2004) and the Meta-Register of Controlled Trials mRCT (October 2004), reference lists and the archive of our working group. We contacted manufacturers of selenium supplements and investigators. SELECTION CRITERIA: Randomised-controlled trials of selenium mono-supplements in cancer patients undergoing tumour specific therapy such as chemotherapy, radiotherapy or surgery. DATA COLLECTION AND ANALYSIS: Two review authors independently checked trials for eligibility, extracted data and assessed trial quality. We sought additional information from investigators when required. MAIN RESULTS: Two trials have been included, a randomised controlled trial with 60 participants at the beginning of the study investigating secondary lymphoedema and an ongoing trial with preliminary results of 63 participants investigating radiotherapy induced diarrhoea as a secondary outcome. Both trials had drawbacks with regard to study quality and reporting. The trial on secondary lymphoedema reported a decreased number of recurrent erysipela infections in the selenium supplementation group compared to placebo. However, results must be interpreted with caution and cannot be generalised to other populations. The ongoing trial on radiotherapy associated diarrhoea preliminarily reported a lower incidence of diarrhoea in patients receiving selenium supplementation concomitant to pelvic radiation, however, no data were presented. Publication of final results must be awaited to discuss these findings in detail. No randomised controlled trials were found studying the effect of selenium supplementation on other therapy-associated toxicities or quality of life or performance status in cancer patients. AUTHORS' CONCLUSIONS: There is insufficient evidence at present that selenium supplementation alleviates the side effects of tumour specific chemotherapy or radiotherapy treatments. Or, that it improves the after effects of surgery, or improves quality of life in cancer patients or reduces secondary lymphoedema. To date research findings do not provide a basis for any recommendation in favour or against selenium supplementation in cancer patients. Potential hazards of supplementing a trace mineral should be kept in mind.

Antineoplastic Agents↗
PubMed2005

Selenium disrupts estrogen signaling by altering estrogen receptor expression and ligand binding in human breast cancer cells.

Cancer prevention studies suggest that selenium is effective in reducing the incidence of cancers including prostate, colon, and lung cancers. Previous reports showed that selenium inhibits premalignant human breast MCF-10AT1 and MCF10AT3B cell growth in vitro and reduces mammary tumor incidence after exposure to carcinogens in tumor models. Because estrogen is critical to the development and differentiation of estrogen target tissues, including the breast, the present study was designed to examine the effect of selenium on estrogen receptor (ER) expression and activation using methylseleninic acid (MSA), an active form of selenium in vitro. Selenium decreased the levels of expression of ERalpha mRNA and protein and reduced the binding of labeled estradiol to estrogen receptor in MCF-7 cells. Selenium inhibited the trans-activating activity of estrogen receptor in MCF-7 cells expressing functional estrogen receptor using a luciferase reporter construct linked to estrogen responsive element. Selenium decreased the binding of estrogen receptor to the estrogen responsive element site using an electrophoretic mobility gel shift assay. Selenium suppressed estrogen induction of the endogenous target gene c-myc. In contrast to the effect on ERalpha in MCF-7 cells, selenium increased ERbeta mRNA expression in MDA-MB231 human breast cancer cells. Thus, differential regulation of ERalpha and ERbeta in breast cancer cells may represent a novel mechanism of selenium action and provide a rationale for selenium breast cancer prevention trial.

Anticarcinogenic Agents↗
PubMed2004

Selenium's effects on MMP-2 and TIMP-1 secretion by human trabecular meshwork cells.

PURPOSE: Because of the observed increase in incidence of glaucoma among some individuals taking selenium as a dietary supplement, the present study was undertaken to investigate mechanisms of selenium-induced changes in homeostasis of human trabecular meshwork (HTM) cells. Specifically, the impact of selenium on matrix metalloproteinases (MMPs), their inhibitors (tissue inhibitors of metalloproteinases; TIMPs), and the second messengers that regulate MMP expression was investigated in an HTM cell culture model. METHODS: HTM cell cultures were treated with an organic selenium compound (methyl seleninic acid), and changes in secretion and activity of MMPs and TIMPs were analyzed by Western blot and zymography. Changes in extracellular-signal-related kinases 1 and 2 (ERK1/2) and phospho-ERK1/2 levels were monitored by Western blot analysis of whole-cell lysates prepared from selenium-treated cells. Photographs of cultures over time were used to document selenium-induced changes in cell morphology. RESULTS: Treatment of HTM cells with selenium for 24 hours at doses ranging from 1 to 10 micro M caused a dose-dependent decrease in the secretion of MMP-2 and TIMP-1. Treatment for 6 hours revealed a significant decrease in MMP-2 and TIMP-1 at the highest dose. MMP-1, -3, and -9 and TIMP-2 were either not detected or their secretion was not consistently influenced by selenium treatment. Selenium treatment caused a significant decrease in ERK1/2 phosphorylation, but no change in overall ERK protein levels. Selenium treatment resulted in dose-dependent, reversible changes in HTM cell-matrix associations. CONCLUSIONS: Selenium-induced changes in MMP-2/TIMP-1 secretion may alter the balance of extracellular matrix turnover in the conventional outflow pathway and cause an increase in intraocular pressure that eventually leads to glaucoma.

Blotting, Western↗
PubMedDate not supplied

The bioavailability of various selenium compounds to a marine wading bird.

The uptake of dietary selenium (about 3.5 mg/kg AF dry wt) as selenomethionine, selenocystine, selenite, selenate, and fish selenium in the plasma and red blood cells (RBC) of the oystercatcher has been investigated. The birds received the various selenium compounds subsequently, for at least 9 wk. After dietary supplementation of selenocystine, selenite, and selenate, plasma selenium was about 350 micrograms/L and RBC selenium 2.1 mg/kg dry wt. After supplementation of selenomethionine, the plasma concentration increased to 630 micrograms/L, and the RBC concentration to 4.1 mg/kg dry wt. When the fodder contained 3.1 mg/kg fish Se, an average plasma and RBC concentration of 415 micrograms/L and 14.4 mg/kg dry wt, respectively, was measured. The maximal increase of the selenium concentration in the plasma was attained at first sampling, 14 d after a change in dietary selenium (selenomethionine or fish Se); the uptake seemed to be a concentration-regulated process. RBC concentrations (Y in mg/kg drug wt) increased with time (X in d) according to Y = a - b e-cX. Fifty percent of the total increase was attained within 17 d, suggesting that diffusion into the RBC played a role. The selenium concentration in the plasma was positively correlated with the (fish)Se concentration in the fodder; the RBC concentration (60 d after the change in diet) was positively correlated with the plasma concentration. When the diet contained fish Se, the blood selenium concentrations of the captive birds were similar to the concentrations measured in field birds. Fish Se is a yet undetermined selenium compound. The present experiment showed that fish Se differed from selenomethionine, selenocystine, selenite, or selenate in uptake from the food and uptake in the RBC.

Animals↗
PubMed1994

Uptake, distribution, and turnover rates of selenium in barley.

The present communication elucidates initially the topographic distribution of selenium in barley grains. Then by the fluorimetric method the uptake of selenium (selenite) in 8-16 d old germinating barley was estimated. Finally by means of 75Se the anabolic and catabolic rates (turnover) of 75Se (selenite) was compared. The distribution of selenium in barley was evaluated after micro-dissection of barley grains. In dried grains the highest concentration was found in husk and pericarp with about 0.6 ppm Se. Then followed Scutellum with 0.4 and 0.3 ppm in embryon. The aleurone layer, embryonic leaves, and initial root did only have 0.2 ppm Se. In order to know more about the uptake and distribution of selenium in 8-d-old barley, the plants were cultivated for a further 8 d in the culture medium with variation in selenite concentration. In roots and leaves, the uptake did not arrive at saturation during the period studied since the dose-response curve increased up to 0.34 mM selenite in the medium, whereas the selenium levels were about 200 ppm in roots and 30 ppm in leaves. However, the uptake was linear, with concentration during 8 d of cultivation up to 0.84 microM selenite for grain and stem. At higher concentrations the dose-response curve diminished its slope. At 0.34 mM selenite the concentration in grain increased to 6.87 ppm and in the stem to 8.13 ppm. The uptake, distribution, and catabolic rate of selenium components in germinating barley were further evaluated by exposing the plants to 0.0492 microCi 75Se (12.6 microM selenite) for up to 4 d. Then the plants were moved to a selenium deficient medium for further 4 d. Then finally the medium was supplemented with high doses of cold selenite (0.126 mM selenite) for further 4 d. The first third period made it possible to estimate the rate of uptake. It was highest in roots (313 fmol/h/mg dw), i.e., about 10 times those of grains, stems, and leaves. The intermediate period where the barley was transferred to a selenium deficient medium made it possible to estimate the kinetics and eventual sparing mechanisms. The selenium losses were highest for leaves (39%), then followed by roots and stems (22 and 25%, respectively). The losses were lowest in grain with 9% Se losses. The losses were three times more pronounced during the first day than in the following 3 d. These data may argue that the selenium is distributed into different pools and that sparing mechanisms may be in function.(ABSTRACT TRUNCATED AT 400 WORDS)

Hordeum↗