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PubMed1991

Selenium metabolism and platelet glutathione peroxidase activity in healthy Finnish men: effects of selenium yeast, selenite, and selenate.

The mean dietary selenium intake in Finland increased from 40 to 100 micrograms/d in 1987 because of the addition in 1985 of selenium to fertilizers. A selenium-supplementation study was performed in 1987 on the same men as were followed in a 1981 study that had a similar design (200 micrograms Se/d). Selenite and selenate, but not selenium yeast increased platelet glutathione peroxidase (GSHPx) activity by 30% compared with placebo, much less than the 70% found in the previous study. Selenium yeast and selenite increased plasma selenium after 11 wk from 1.39 mumol/L to peak values of 2.15 and 1.58 mumol/L, respectively. Only yeast selenium was incorporated into red cells. From a regression plot based on present and literature data, it was estimated that the plasma selenium concentration needed to achieve maximal platelet GSHPx activity was 1.25-1.45 mumol/L. At the present selenium intake in Finland, 100 micrograms/d, GSHPx activity is saturated in plasma and red cells and almost saturated in platelets.

Analysis of Variance↗
PubMed1991

Selenium distribution in blood fractions of New Zealand women taking organic or inorganic selenium.

Three groups of 11 New Zealand women each received, for 32 wk, yeast tablets with no added selenium (placebo) or 200 micrograms Se/d in tablets either as selenate or as selenium-enriched yeast (SeMet) in a double-blind selenium trial. Plasma and erythrocyte (RBC) samples were collected bimonthly. Gel filtration of plasma from women taking SeMet revealed two major selenium-containing peaks with most of the selenium in the second peak. In contrast, the first peak contained most of the selenium in plasma from women taking selenate. Chromatography of RBC lysates indicated that the majority of the selenium was with hemoglobin (Hb) in women taking SeMet but was about equally distributed between glutathione peroxidase (GSH-Px) and Hb in women taking selenate. The percentage of selenium associated with GSH-Px was found to be greater in RBCs and plasma of women taking selenate than of those taking SeMet.

Adult↗
PubMed1995

Selenate fortification improves selenium status of term infants fed soy formula.

Thirty-three healthy term infants were fed either soy formula (SF, 0.028 mumol Se/L; n = 17) or soy formula with added selenate (SF+Se, 0.17 mumol Se/L; n = 16) from birth (+4 d) to 16 wk. Selenium intakes of infants fed SF+Se were similar to the recommended dietary allowance and significantly greater than those of SF-fed infants. The SF group had significantly lower plasma, erythrocyte, and urine selenium, and lower plasma and erythrocyte glutathione peroxidase (GPx) activities at 16 wk compared to those of infants fed SF+Se. A decrease in plasma selenium was observed in SF-fed infants, whereas no differences in plasma selenium were found in infants fed SF+Se. These results indicate that selenate added to soy formula is highly available and effective at maintaining infant plasma and erythrocyte selenium concentrations and GPx activities that are greater than those of infants fed soy formula not fortified with selenium.

Double-Blind Method↗
PubMed1996

Selenate fortification of infant formulas improves the selenium status of preterm infants.

The purpose of this study was to determine whether selenate fortification of infant formula would improve the selenium status of relatively well, growing, preterm infants during the first 12 wk of enteral feeding. A high-selenium group (n = 7, mean body weight = 1312 g) received selenate-fortified preterm and full-term infant formulas containing 0.36 and 0.22 mumol Se/L, respectively, and a low-selenium group (n = 10, mean body weight = 1262 g) received non-selenium-fortified preterm and full-term infant formulas containing 0.12 and 0.11 mumol Se/L, respectively. There were no significant differences in growth between the two groups throughout the study. The high-selenium group had significantly greater mean selenium intakes than did the low-selenium group from weeks 2 to 12. Plasma selenium concentrations decreased over the study period in the low-selenium group. Plasma selenium-dependent glutathione peroxidase activity was greater in the high-selenium group at week 12 only. Red blood cell selenium concentrations decreased over time in both groups and were significantly greater in the high-selenium group at weeks 4, 8, and 12. Plasma selenium concentrations were significantly correlated with plasma glutathione peroxidase activity for all infants on study day 1 and at weeks 4 and 12. Selenium intake of all infants was significantly correlated with plasma glutathione peroxidase activity at 12 wk. Selenate fortification of infant formulas can improve the selenium status of preterm infants. Current selenium contents of infant formulas and recommendations for dietary intakes of selenium for some preterm infants may be inadequate.

Anthropometry↗
PubMed1982

Evaluation of the effect of sodium selenate on the growth of mycobacterial stock cultures.

A study was undertaken to evaluate the effect of sodium selenate supplementation (5 micrograms/mL) on the growth characteristics of a variety of mycobacterial isolates. Supplemented Lowenstein-Jensen and Middlebrook 7H11 agar were compared to nonsupplemented media. Eighteen mycobacterium stock isolates were tested. Selenate supplementation had no predictable or consistent growth stimulatory effect as compared with nonsupplemented media.

Bacteriological Techniques↗
PubMedDate not supplied

Randomized comparative clinical trial of itraconazole and selenium sulfide shampoo for the treatment of pityriasis versicolor.

Forty patients with pityriasis versicolor, fluorescence of involved areas under Wood's light, and positive microscopic identification of Malassezia furfur were randomly assigned to treatment with either oral itraconazole (200 mg once daily for five consecutive days) or 2.5% selenium sulfide shampoo (once daily application for seven days). Each treatment group consisted of 20 patients. On assessment three weeks after the end of treatment, all patients given itraconazole showed a response: 17 were healed, and three had mild residual lesions. Likewise, all patients in the selenium sulfide group responded to therapy: 16 were healed, and four had mild residual lesions. Tolerability, acceptability, and compliance were excellent with itraconazole. All 20 patients given the drug stated a preference for oral treatment. In the selenium sulfide group, five patients (25%) had adverse reactions attributable to the medication; one of these patients experienced an irritation severe enough to warrant the discontinuation of treatment on the third day. Ten patients in this group stated a preference for oral treatment.

Administration, Oral↗
PubMed1985

In vivo intestinal absorption of selenate and selenite by rats.

Intestinal absorption of selenate and selenite was investigated in rats by using an in vivo perfusion technique. Different segments of the intestine were perfused with an isotonic solution containing different concentrations of SeO42- or SeO32-. The site of greatest SeO42- absorption was found to be the ileum followed in descending order by the proximal jejunum and large intestine (cecum and colon). Furthermore, SeO42- was absorbed significantly faster from the ileum than SeO32-. The concentration dependence of SeO42- absorption indicates that SeO42- is absorbed by a saturable transport mechanism of the ileal mucosa. Absorption of SeO42- at a concentration of 0.01 mM was not affected by the presence of 1 mM SeO42- in the perfusate. When the SeO42- concentration of the perfusate was increased to 1 mM, the absorptive functions of the ileal epithelium appeared to be generally impaired. It is concluded that selenate is absorbed from the ileum by a carrier-mediated mechanism.

Animals↗
PubMed1985

Active absorption of selenate by rat ileum.

Intestinal absorption of selenate and selenite in rats was investigated in vitro by using everted sacs of the duodenum, jejunum and ileum. Only the ileal sacs incubated with selenate accumulated selenium in the serosal fluid during the incubation. Selenium transport across the ileum did not occur against a concentration gradient when selenite instead of selenate was present in the incubation medium. Sulfate and thiosulfate significantly inhibited ileal selenate transport. Decreasing the activity of the Na+,K+-ATPase, by the addition of ouabain, resulted in a significant reduction of concentrative selenate transport by the ileum. Furthermore L-leucine, but not D-glucose and D-galactose, significantly reduced selenium absorption by ileal sacs incubated with selenate. It is concluded from these results that selenate is transported actively by the ileal mucosa and that a common transport mechanism for selenate and sulfate exists. The Na+-gradient across the intestinal brush border membrane seems to be capable of energizing active ileal selenate transport.

Animals↗
PubMed1988

Nutritional availability and chronic toxicity of selenocyanate in the rat.

To evaluate nutritional availability and chronic toxicity of KSeCN, female postweanling rats were fed casein-based diets plus 0.1, 0.5, 2.5, 5 and 10 mg Se/kg as KSeCN for 6 wk, or 0.1, 0.5 and 10 mg Se/kg as Na2SeO3. A control group was fed the basal diet (Se = 0.04 mg/kg) and one group was fed the basal diet plus 5 mg Se/L as KSeCN in the drinking water. There were no differences in weight gain and diet consumption among groups fed 2.5 mg Se/kg or less. At 5 and 10 mg Se/kg, rats showed depression in weight gain and diet consumption. After wk 6 there were no abnormalities of the major organs of rats fed 2.5 mg Se/kg or less. Spleen enlargement was observed at 5 and 10 mg Se/kg, and liver damage and kidney enlargement at 10 mg Se/kg. Se content in the blood, liver and kidney of rats fed KSeCN was generally somewhat lower than for those fed Na2SeO3 at the same levels. The availability of Se from KSeCN for glutathione peroxidase formation in blood, liver and kidney was comparable to that of Na2SeO3. Plasma thyroxine in groups fed 10 mg Se/kg was 40% of that in the control group, but was not altered at lower Se levels.

Animals↗
PubMed1990

Comparative toxicity and tissue retention of selenium in methionine-deficient rats fed sodium selenate or L-selenomethionine.

Selenium (Se) toxicity is known to be affected by level of intake of the mineral, but there are conflicting reports on the relative toxicities of the various chemical forms of Se. We monitored Se toxicity in rats fed Torula yeast-based diets containing 0.1, 0.5 or 2.5 micrograms Se/g of diet as either sodium selenate (Na2SeO4) or L-selenomethionine (SeMet). Half the diets were supplemented to contain adequate dietary methionine (Met). Weights were monitored weekly for 6 (Met-adequate) or 7 (Met-deficient) wk, at which time the rats were killed. There were no significant differences in final weight among Met-adequate rats, regardless of level or form of dietary Se. Methionine-deficient rats all gained significantly less weight than their Met-adequate counterparts. Selenosis was most severe in the Met-deficient rats fed 2.5 micrograms Se/g of diet as Na2SeO4, as indicated by significantly impaired weight gains. Nonetheless, Se retention in serum, heart, brain, bone, testes, colon, skin, lungs and pancreas was greater in rats fed SeMet than in those fed Na2SeO4, and Met deficiency further intensified this trend. The kidney was the only organ in which Se levels were markedly higher in the severely poisoned Met-deficient rats fed Na2SeO4. Further research is needed to determine whether elevated kidney Se levels are related to the greater toxicity observed in the Met-deficient rats fed Na2SeO4.

Animals↗
PubMed2002

Antioxidant regulation of protein kinase C in cancer prevention.

Besides scavenging free radicals, antioxidants inhibit signaling enzymes such as protein kinase C (PKC) that play a crucial role in tumor promotion. By having different oxidation susceptible regions, PKC can respond to both oxidant tumor promoters and cancer-preventive antioxidants to elicit opposite cellular responses. Oxidant tumor promoters activate PKC by reacting with zinc-thiolates present within the regulatory domain. In contrast, the oxidized forms of some cancer-preventive agents, such as polyphenolics (ellagic acid, 4-hydroxytamoxifen and curcumin) and selenocompounds, can inactivate PKC by oxidizing the vicinal thiols present within the catalytic domain. This brings an efficient counteractive mechanism to block the signal transduction induced by tumor promoters at the first step itself. Because prostate cancer prevention clinical trials in large human population are under way, we have focused more on understanding the cancer-preventive mechanism of selenium. Methylselenol, the postulated cancer-preventive metabolite, has no direct effect on PKC activity. However, methylseleninic acid, locally generated by the reaction of membrane methylselenol with PKC-bound tumor-promoting fatty acid hydroperoxides, selectively inactivates PKC. This mechanism clarifies how the volatile methylselenol that is present in a low concentration induces the inactivation of PKC selectively in the promoting precancer cells. Selenoprotein thioredoxin reductase reverses selenium-induced inactivation of PKC, suggesting that selenoproteins may serve as a safeguard against the toxicity induced by selenometabolites. Moreover, this also explains how a resistance to selenium develops in advanced malignant cells. The redox-mediated inactivation of PKC may, at least in part, be responsible for the antioxidant-induced inhibition of tumor promotion and cell growth, as well as for the induction of cell death.

Animals↗
PubMed2003

Effects of dietary selenium supplementation on DNA damage and apoptosis in canine prostate.

The trace mineral selenium inhibits cancer development in a variety of experimental animal models. We used an in vivo canine model to evaluate the effects of dietary selenium supplementation on DNA damage in prostate tissue and on apoptosis in prostate epithelial cells. Sexually intact elderly male beagle dogs were randomly assigned to receive an unsupplemented diet (control group) or diets that were supplemented with selenium (treatment group), either as selenomethionine or as high-selenium yeast at 3 micro g/kg or 6 micro g/kg body weight per day for 7 months. The extent of DNA damage in prostate cells and in peripheral blood lymphocytes, as determined by the alkaline comet assay, was lower among the selenium-supplemented dogs than among the control dogs (prostate P<.001; peripheral blood lymphocytes P =.003; analysis of variance) but was not associated with the activity of the antioxidant enzyme glutathione peroxidase in plasma. The median number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive (i.e., apoptotic) prostate epithelial cells was 3.7 (interquartile range = 1.1-7.6) for the selenium-supplemented dogs and 1.7 (interquartile range = 0.2-2.8) for the control dogs ( P =.04, Mann-Whitney U test). These data suggest that dietary selenium supplementation decreases DNA damage and increases epithelial cell apoptosis within the aging canine prostate.

Animals↗
PubMed2004

Selenium and colorectal adenoma: results of a pooled analysis.

BACKGROUND: Secondary analyses of data from a large randomized clinical trial have suggested that intake of the trace element selenium reduces risk of colorectal neoplasia, but epidemiologic studies have not shown a consistent protective association. METHODS: We conducted a combined analysis of data from three randomized trials--the Wheat Bran Fiber Trial, the Polyp Prevention Trial, and the Polyp Prevention Study--which tested the effects of various nutritional interventions for colorectal adenoma prevention among participants who recently had an adenoma removed during colonoscopy. Selenium concentrations were measured from blood specimens from a total of 1763 trial participants, and quartiles of baseline selenium were established from the pooled data. To estimate the association between baseline selenium and colorectal adenoma risk, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression modeling. All statistical tests were two-sided. RESULTS: Individual study results among participants whose blood selenium concentrations were in the highest versus the lowest quartile varied in magnitude (Polyp Prevention Trial: OR = 0.67, 95% CI = 0.43 to 1.05; P(trend) = .21; Wheat Bran Fiber Trial: OR = 0.66, 95% CI = 0.40 to 1.10; P(trend) = .13, and Polyp Prevention Study: OR = 0.57, 95% CI = 0.34 to 0.95, P(trend) = .04). Analyses of the pooled data showed that individuals whose blood selenium values were in the highest quartile (median = 150 ng/mL) had statistically significantly lower odds of developing a new adenoma compared with those in the lowest quartile (OR = 0.66, 95% CI = 0.50 to 0.87; P(trend) = .006). CONCLUSIONS: The inverse association between higher blood selenium concentration and adenoma risk supports previous findings indicating that higher selenium status may be related to decreased risk of colorectal cancer.

Adenoma↗
PubMed1996

The protective role of glutathione peroxidase in apoptosis induced by reactive oxygen species.

Selenium-dependent glutathione peroxidase (GPx) plays a protective role in oxidative stress-induced apoptosis. In this study, we demonstrated that MDBK cells, a bovine renal epithelial cell line, exhibited internucleosomal DNA fragmentation characteristic of apoptotic cell death under selenium-deficient conditions with lower doses of hydrogen peroxide (H2O2) than under selenium-supplemented ones. This was due to a decreased amount of GPx in the cells under selenium-deficient conditions, because other antioxidative enzyme activities were not affected by the selenium supplementation. Cumene hydroperoxide also induced DNA fragmentation in selenium-deficient cells but no ladder formation was observed. Flow cytometric analysis showed that selenium-deficient cells were less capable of scavenging intracellular peroxides after exposure to exogenous H2O2 than selenium-supplemented ones. In contrast, there was no difference in viability between selenium-supplemented and non-supplemented cells in cell survival after exposure to menadione, which activates the electron transport system and increases intracellular superoxide radicals. Clofibrate, a peroxisomal proliferator and an inducer of catalase (CAT), partially protected both Se-deficient and Se-supplemented cells from exogenous H202. We concluded that selenium-deficient cells were more easily brought to apoptotic cell death by peroxides, but not by superoxide radicals, than selenium-supplemented ones and that CAT could compensate for the depletion of GPx to a certain degree by scavenging H2O2.

Animals↗
PubMed2005

Broiler breeder semen quality as affected by trace minerals in vitro.

Research has shown that trace elements, such as Se, Mn, and Zn, can alter reproductive functions. The aim of the current study was to evaluate the sperm quality index (SQI) and sperm viability as affected by various levels and sources of Se, Mn, and Zn when added in vitro to broiler breeder semen. In vitro treatments consisted of the following sources and levels of minerals: Control, no minerals added to sperm; seleno L-methionine, 4 levels ranging from 8.78 to 7,896 microg/L; sodium selenite, 4 levels ranging from 8.78 to 7,896 microg/L; MnSO4, 8 levels ranging from 6,500 to 65,000 mg/L; Zn 180 (Zinpro Corporation), 4 levels ranging from 0.65 to 650 mg/L; and ZnSO4, 4 levels ranging from 0.65 to 650 mg/L. The addition of 7,896 microg of sodium selenite/L to semen was detrimental to sperm motility. Also, MnSO4 adversely affected SQI and sperm viability at concentrations of 6,500 mg/L and greater. Sperm viability was decreased when 650 mg/L of Zn 180 was added to semen. Sperm motility was depressed by exposure to Zn 180 at 650 mg/L and ZnSO4 at 65 and 650 mg/L. Our results suggest that these trace minerals must act at the reproductive tissue level during spermatogenesis to improve semen quality. Direct in vitro application of these elements to semen appears to be detrimental to spermatozoa.

Animals↗