Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Selenium”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,405 records · Page 78Linked to original sources
PubMed2004

Prospective study of serum selenium concentrations and esophageal and gastric cardia cancer, heart disease, stroke, and total death.

BACKGROUND: We previously reported an inverse association between prediagnostic serum selenium concentrations and the risk of esophageal squamous cell carcinoma (ESCC) and gastric cardia cancer (GCC) but not gastric noncardia cancer (GNCC) in a nested study from the Nutrition Intervention Trial in Linxian, China. OBJECTIVE: We examined the relation between baseline serum selenium and the subsequent risk of death from ESCC, GCC, GNCC, heart disease (HD), stroke, and total death over 15 y of follow-up (1986-2001). DESIGN: We measured baseline serum selenium concentrations in 1103 subjects randomly selected from a larger trial cohort. We identified 516 deaths during the 15-y follow up, including 75 from ESCC, 36 from GCC, 116 from HD, and 167 from stroke. Relative risks (RRs) and 95% CIs were estimated by using Cox proportional hazards regression models. Reported RRs estimated the change in risk conferred by a 25% increase in serum selenium relative to the population distribution. All estimates were adjusted for sex, age, smoking, drinking, and serum cholesterol. RESULTS: We found significant inverse associations between baseline serum selenium and death from ESCC (RR: 0.83; 95% CI: 0.71, 0.98) and GCC (0.75; 0.59, 0.95). Trends toward inverse associations were noted for death from HD (0.89; 0.78, 1.01; P = 0.07), but no association was noted for total death (0.96; 0.90, 1.02) or stroke (0.99; 0.88, 1.11). CONCLUSION: Population-wide selenium supplementation in the region of China with low serum selenium and high incidences of ESCC and GCC merits serious consideration.

Adult↗
PubMed2006

Effects of selenium supplementation on cardiovascular disease incidence and mortality: secondary analyses in a randomized clinical trial.

Despite the documented antioxidant and chemopreventive properties of selenium, studies of selenium intake and supplementation and cardiovascular disease have yielded inconsistent findings. The authors examined the effect of selenium supplementation (200 microg daily) on cardiovascular disease incidence and mortality through the entire blinded phase of the Nutritional Prevention of Cancer Trial (1983-1996) among participants who were free of cardiovascular disease at baseline (randomized to selenium: n = 504; randomized to placebo: n = 500). Selenium supplementation was not significantly associated with any of the cardiovascular disease endpoints during 7.6 years of follow-up (all cardiovascular disease: hazard ratio (HR) = 1.03, 95% confidence interval (CI): 0.78, 1.37; myocardial infarction: HR = 0.94, 95% CI: 0.61, 1.44; stroke: HR = 1.02, 95% CI: 0.63, 1.65; all cardiovascular disease mortality: HR = 1.22, 95% CI: 0.76, 1.95). The lack of significant association with cardiovascular disease endpoints was also confirmed when analyses were further stratified by tertiles of baseline plasma selenium concentrations. These findings indicate no overall effect of selenium supplementation on the primary prevention of cardiovascular disease in this population.

Cardiovascular Diseases↗
PubMed1981

Anticarcinogenic effect of selenium in rats treated with dimethylbenz[a]anthracene and fed different levels and types of fat.

The present investigation reports the effect of selenium supplementation on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in rats fed either a 5% or a 25% corn oil diet. A reduction in tumorigenesis in both groups was observed with 2.5 p.p.m. of dietary selenium. Selenium supplementation also inhibited the development of hyperplastic alveolar nodules in the mammary gland subsequent to DMBA treatment. In addition, the appearance of mammary neoplasia was reduced by selenium in rats fed a high-saturated fat diet (coconut oil), indicating that the type of fat consumed did not influence the antitumorigenic effectiveness of selenium. The lack of a correlation between the anticarciongenic efficacy of selenium and its ability to suppress lipid peroxidation in the mammary tissue of rats fed either a high-saturated fat or a high-unsaturated fat diet suggests that the inhibitory action of selenium is probably not mediated by its antioxidant function in lipid metabolism

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1998

Selenium in human male reproductive organs.

The objective of the study was to obtain information on the concentration and distribution of selenium throughout the human male reproductive tract. Material was removed at autopsy from 41 men who had died suddenly and unexpectedly. Semen samples were also provided from 184 men attending an andrology clinic for fertility investigation and from 32 healthy volunteers. Significant positive correlations in the selenium concentration were demonstrated between the different reproductive organs, the testis having the highest concentrations. No correlation was found between the concentration of selenium in the genital organs and liver, kidney or blood, suggesting that its uptake and/or biochemical activity in the reproductive organs may be controlled by similar mechanisms not shared by the other organs. No significant age-dependent changes could be detected in tissue selenium concentrations. In a group of men under fertility investigation, a significant positive correlation was obtained between seminal plasma concentrations of selenium and concentrations of spermatozoa in the same ejaculate. A significant positive correlation between concentrations of zinc and selenium in the same ejaculates indicated that selenium may arise largely from the prostate gland.

Adolescent↗
PubMed1975

Selenium levels in human blood and tissues in health and in disease.

The levels of selenium in human sera and pancreatic, hepatic and synovial tissues were measured. An attempt was made to correlate the selenium level with certain disease states. Selenium was determined by nerutron activation analysis, using the 17.4 second half-life isotope 77mSe with a sensitivity of 2ppb. Serum-bound selenium was determined in normal individuals and individuals with various malignancies, and medical and surgical disorders. Tissue selenium was assayed in diseased and normal pancreases, livers, and synovial membranes. A wide variation was observed both in the serum selenium content of patients with a malignancy and in postmoren pancreatic and synovial showing histopathological changes. Significantly lower selenium values were observed in sera from cancer patients than from normal individuals. Higher values were generally observed in patients with primary neoplasms of the reticuloendothelial system. Higher tissue concentrations were obtained in synovia from patients with rheumatoid arthritis and in pancreatic tissues associated with histopathological changes.

Arthritis, Rheumatoid↗
PubMed1976

Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs.

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.

Animals↗
PubMed1976

Influence of ascorbic acid on selenium nutrition in the chick.

Experiments were conducted to determine the nature of the effect of dietary ascorbic acid on selenium nutrition in the chick. Results showed that ascorbic acid resulted in increased activities of the selenium-containing enzyme glutathione peroxidase in plasma, accompanied by an apparent reduction in the dietary selenium requirement of the vitamin E-deficient chick. The ascorbic acid contents of plasma, liver, kidney and adrenals were not affected by selenium or vitamin E deficiencies, indicating that selenium-vitamin E deficient chicks are not rendered scrobutic. Absorption experiments using ligated duodenal loops or oral doses indicated that dietary ascorbic acid promoted the enteric absorption of selenium but did not affect the absorption of vitamin E. These results support the hypothesis previously reported that factors which inhibit the oxidation of dietary selenium promote its absorption and, perhaps, its post-absorptive utilization in metabolically active components of the cell.

Animals↗
PubMed1977

Selenosis, hepatic selenium accumulation, and plasma glutathione peroxidase activity in chicks as affected by a factor in linseed meal.

Linseed meal has previously been reported to contain an organic factor that reduces toxicity of selenium in animals. The purpose of the studies reported here was to obtain information on the mechanism of action of the linseed meal factor in counteracting selenosis in chicks. Feeding a diet containing 20% linseed meal to chicks partially counteracted the growth depression caused by including high levels of selenium (10-40 ppm) in the diet. In contrast to the rat, chicks fed diets containing selenium did not accumulate significantly more of the element per unit of liver dry matter when the diet contained linseed meal, and at two selenium levels accumulated significantly less. Linseed meal did not interfere with the absorption of an oral dose of 75Se as measured by tissue retention 24 hours later. A methanol extract of linseed meal did not interfere with the normal increase in plasma glutathione peroxidase activity in chicks fed diets supplemented with low levels of selenium even though the extract counteracted the growth depression obtained by adding 20 ppm selenium. Linseed meal contains a factor that interacts with selenium in the tissues in some unknown way to reduce the toxic effects of the element, but does not prevent normal synthesis of glutathione peroxidase.

Animals↗
PubMed1983

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

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.

Animals↗
PubMed1985

Effect of selenium deficiency on hydroperoxide-induced glutathione release from the isolated perfused rat heart.

Selenium deficiency has been implicated as a cause of the cardiomyopathy known as Keshan disease in China. Selenium is an essential constituent of glutathione peroxidase, an enzyme that destroys hydroperoxides by using the reducing equivalents of reduced glutathione (GSH). We studied glutathione-dependent hydroperoxide metabolism in isolated perfused rat hearts. Hearts from selenium-deficient rats contained 5% of the glutathione peroxidase activity found in control hearts. Glutathione reductase activity and glutathione content were not affected by selenium deficiency. Infusion of t-butylhydroperoxide into control hearts caused an increase in heart glutathione disulfide (GSSG) concentration proportional to the rate of hydroperoxide infusion up to 200 nmol/(g heart X min). GSSG was released into the perfusate in proportion to the hydroperoxide infusion rate up to 150 nmol/(g heart X min), but GSSG release did not increase further with higher infusion rates. Thus, GSSG release by the heart is saturable. It had a maximum rate of about 14 nmol GSH equivalents/(g heart X min) when stimulated by t-butylhydroperoxide infusion. This indicates that GSSG release by the heart is carrier-mediated and is not due to passive diffusion. Infusion of hydroperoxide into selenium-deficient hearts failed to cause increases in heart GSSG concentration and in GSSG release. This indicates that selenium-deficient heart cannot metabolize hydroperoxides through glutathione-dependent pathways. We suggest that selenium deficiency might predispose the heart to injury from oxidant stress.

Animals↗
PubMed1986

Effects of singular and combined dietary deficiencies of selenium and vitamin E on fingerling channel catfish (Ictalurus punctatus).

Selenium and vitamin E interrelationships in the nutrition of channel catfish (Ictalurus punctatus) were investigated in a 26-wk experiment. A purified basal diet alone or supplemented with 0.2 mg/kg selenium, 50 mg/kg vitamin E or both was fed to fingerling channel catfish in aquaria. Combined deficiencies of selenium and vitamin E caused suppressed growth, anemia, severe myopathy, exudative diathesis and death. Singular deficiencies of either selenium or vitamin E did not produce any of these deficiency signs. Catfish fed selenium-deficient diets with or without supplemental vitamin E had reduced glutathione peroxidase activity and elevated glutathione transferase activity in liver. Vitamin E deficiency in catfish caused elevated ascorbic acid-stimulated lipid peroxidation of hepatic microsomes, which was unaffected by selenium supplementation. The results indicate that there is a significant interaction between selenium and vitamin E in the nutrition of the channel catfish.

Animals↗
PubMed1989

Upper limit of selenium in infant formulas.

At present, the amount of selenium in infant formulas is not controlled and varies depending upon the selenium content of the raw materials used in its manufacture. Since selenium deficiency has been associated with two diseases of childhood, prudence dictates that the concentration of selenium in infant formula be standardized. Extrapolation from studies with human adults indicates that a daily intake of 10 microg of selenium is sufficient to meet the nutritional requirement of the infant while providing a reasonable margin of safety. Extrapolation from adult studies also suggests that intakes of 75-160 microg/d might have harmful effects in infants. On the other hand, no cases of selenosis in infants have been reported in high selenium areas of the United States, where human breast milk supplies as much as 47 microg/d. Therefore, it is proposed that infant formulas contain enough selenium to provide 10-45 microg/d.

Female↗
PubMed1991

Effect of chemical form of selenium on tissue glutathione peroxidase activity in developing rats.

Two experiments were conducted to determine the effect of various forms of selenium (Se) on the activity of glutathione peroxidase (GSHPx) in liver, heart, kidney and eyes of the developing rat. In experiment 1, throughout mating, pregnancy and lactation, female rats consumed one of three diets: basal (less than 0.05 microgram Se/g); selenite (0.15 microgram Se/g) and selenomethionine (0.15 microgram Se/g). Some pups born to dams in the basal group were also given intraperitoneal doses of saline, selenite or selenomethionine. GSHPx activity was measured in tissues from fetuses, 7-d-old and 14-d-old nursing pups and the dams. In all tissues studied, GSHPx activity was highest in the 14-d-old pups whose mothers were in the selenomethionine group. Rat pups given intraperitoneal selenite (3 micrograms/kg body weight) had higher liver and kidney GSHPx activity than pups given the same amount of selenium as intraperitoneal selenomethionine. In experiment 2, all dams were fed the same basal diet, and pups were weaned to diets containing one of two levels of selenium (0.1 or 0.2 microgram/g), one of three forms of selenium (selenite, selenomethionine or selenocystine) or no added selenium. After 14 d of repletion, the highest level of hepatic GSHPx activity occurred in the selenite group and the lowest in the basal diet group. After 21 d of repletion, renal GSHPx activity was lowest in the basal group followed by the selenocystine group. The highest tissue selenium concentration was found in kidney tissues of the selenocystine group. These data support the hypothesis that these dietary forms of selenium are differentially available for GSHPx activity.

Animals↗
PubMed1991

Effects of dietary selenium and fish oil (MaxEPA) on arachidonic acid metabolism and hemostatic function in rats.

This study investigated whether hemostatic function can be modified by both the consumption of fish oil and the level of dietary selenium. Male Sprague-Dawley rats were fed for 8 wk semipurified diets containing 7% corn oil (by wt) or 5.5% fish oil (MaxEPA) plus 1.5% corn oil with or without selenium supplementation. Consumption of the four diets caused no difference in weight gain, food intake or plasma malondialdehyde content. The selenium-supplemented rats had significantly higher levels of selenium and glutathione peroxidase activity in plasma. Fish oil feeding decreased ADP-induced platelet aggregation and increased bleeding time. The level of dietary selenium and type of oil interacted to influence the production of 6-keto-prostaglandin F1 alpha: more was produced when corn oil was fed in the selenium-deficient diets. These data suggest that the effect of dietary selenium on hemostatic function and the production of eicosanoids is minor.

Administration, Oral↗
PubMed1998

Lessons from basic research in selenium and cancer prevention.

The article reviews the progress in basic research of selenium and cancer prevention during the past decade. Special emphasis is placed on the following four major areas of discussion: 1) chemical forms of selenium and anticarcinogenic activity; 2) selenium-enriched food; 3) in vitro effects of selenite vs. monomethylated selenium; and 4) aromatic selenium compounds. It is clear that basic research has contributed new knowledge to our understanding of selenium biochemistry, anticancer efficacy and regulation of cell growth. Some of this information could be ready for incorporation into the design of a second-generation selenium trial in humans.

Anticarcinogenic Agents↗
PubMed2003

Dietary folate and selenium affect dimethylhydrazine-induced aberrant crypt formation, global DNA methylation and one-carbon metabolism in rats.

Several observations suggest a role for DNA methylation in cancer pathogenesis. Although both selenium and folate deficiency have been shown to cause global DNA hypomethylation and increased cancer susceptibility, the nutrients have different effects on one-carbon metabolism. Thus, the purpose of this study was to investigate the interactive effects of dietary selenium and folate. Weanling, Fischer-344 rats (n = 23/diet) were fed diets containing 0 or 2.0 mg selenium (as selenite)/kg and 0 or 2.0 mg folate/kg in a 2 x 2 factorial design. After 3 and 4 wk of a 12-wk experiment, 19 rats/diet were injected intraperitoneally with dimethylhydrazine (DMH, 25 mg/kg) and 4 rats/diet were administered saline. Selenium deficiency decreased (P < 0.05) colonic DNA methylation and the activities of liver DNA methyltransferase and betaine homocysteine methyltransferase and increased plasma glutathione concentrations. Folate deficiency increased (P < 0.05) the number of aberrant crypts per aberrant crypt foci, the concentration of colonic S-adenosylhomocysteine and the activity of liver cystathionine synthase. Selenium and folate interacted (P < 0.0001) to influence one-carbon metabolism and cancer susceptibility such that the number of aberrant crypts and the concentrations of plasma homocysteine and liver S-adenosylhomocysteine were the highest and the concentrations of plasma folate and liver S-adenosylmethionine and the activity of liver methionine synthase were the lowest in rats fed folate-deficient diets and supplemental selenium. These results suggest that selenium deprivation ameliorates some of the effects of folate deficiency, probably by shunting the buildup of homocysteine (as a result of folate deficiency) to glutathione.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2004

The link between selenium and chemoprevention: a case for selenoproteins.

Selenium is effective in reducing cancer incidence in animal models, and epidemiologic data, as well as supplementation trials, have indicated that selenium is likely to be effective in humans. The mechanism by which selenium prevents cancer remains unknown. The mammalian genome encodes 25 selenoprotein genes, each containing one or more molecules of selenium in the form of the amino acid selenocysteine, translationally inserted into the growing peptide in response to the UGA codon. There is evidence that several of these proteins may be involved with the mechanism by which selenium provides its anticancer effects. Data are reviewed indicating that genetic variants of the cytosolic glutathione peroxidase are associated with increased cancer risk, and that loss of one of the copies of this same gene may be involved with malignant progression. Similarly, allelic differences in the gene for a second selenoprotein, Sep15, may be relevant to the protection provided by selenium, and allelic loss at this locus have been reported as well. These data, along with the differential expression patterns reported for other selenoproteins in tumor vs. normal tissues, support the role of selenoproteins in the chemoprotection by selenium.

Animals↗
PubMed2004

Serum selenium is associated with plasma homocysteine concentrations in elderly humans.

Low selenium levels in humans have been associated with several pathologies; however, an earlier animal investigation found a direct association between Se intake and total plasma homocysteine (tHcy) concentrations. To date, the importance of serum selenium levels in association with tHcy in humans has not been determined. We evaluated the cross-sectional association of blood selenium concentrations with plasma tHcy and other determinants of this cardiovascular disease risk factor. We estimated protein intake and measured the blood status of selenium, tHcy, and several other related factors in serum such as folate, vitamin B-12, and creatinine. Serum selenium was inversely associated with tHcy, explaining 5.8% of tHcy variance with respect to 2.2% accounted for by serum folate. Furthermore, there was a 63% decreased risk of higher tHcy concentrations (>14 micro mol/L) for subjects with serum selenium in the highest tertile (P = 0.013). We also found an inverse association of protein intake with tHcy in men (beta = -0.144; P = 0.036), which disappeared after controlling for serum Se concentrations (beta = -0.055; P = 0.003). In conclusion, selenium should be considered as a potential factor to lower tHcy. In addition, the described association between protein intake and homocysteine levels could be mediated by this trace element.

Aged↗