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PubMed2004

Dimethylselenide demethylation is an adaptive response to selenium deprivation in the archaeon Methanococcus voltae.

The archaeon Methanococcus voltae needs selenium for optimal growth. A gene group most likely involved in the demethylation of dimethylselenide was discovered, the expression of which is induced upon selenium deprivation. The operon comprises open reading frames for a corrinoid protein and two putative methyltransferases. It is shown that the addition of dimethylselenide to selenium-depleted growth medium relieves the lack of selenium, as indicated by the repression of a promoter of a transcription unit encoding selenium-free hydrogenases which is normally active only upon selenium deprivation. Knockout mutants of the corrinoid protein or one of the two methyltransferase genes did not show repression of the hydrogenase promoter in the presence of dimethylselenide. The mutation of the other methyltransferase gene had no effect. Growth rates of the two effective mutants were reduced compared to wild-type cells in selenium-limited medium in the presence of dimethylselenide.

Adaptation, Physiological↗

PubMed1980

Selenium-dependent enzymes.

Selenium, molecular weight 78.96, resembles sulfur in many of its chemical properties and occurs in inorganic forms as H2Se, H2Se2O3, H2SeO3, and H2SeO4 which are the analogues of hydrogen sulfide, thiosulfate, sulfite, and sulfate, respectively. The commonly available radionuclide, 75Se, is a gamma emitter (half-life 122 days) that is used extensively as a tracer in biochemical studies and as a radiopharmaceutical agent for diagnostic purposes. Organoselenium compounds, in general, are less stable and more reactive than the corresponding sulfur analogues and these properties may account for the toxicity of selenium when it is incorporated indiscriminately in place of sulfur in cellular constituents. On the other hand living systems may have exploited the greater reactivity of certain types of organoselenium compounds in those instances where selenium is specifically required as a component of an enzyme or other macromolecule. Several enzymic processes that do not distinguish selenium from sulfur and therefore may be important in selenium toxicity were discussed in some detail in two earlier reviews on selenium biochemistry (1, 2) and this aspect of the problem is not treated here. Rather, the information currently available on the properties and catalytic functions of the four known selenium-dependent enzymes is summarized. These enzymes are formate dehydrogenases of Escherichia coli and several anaerobic bacteria, clostridial glycine reductase, mammalian and avian glutathione peroxidase, and nicotinic acid hydroxylase of Clostridium barkeri. Additional selenoproteins whose catalytic activities are as yet unidentified are mentioned.

Aldehyde Oxidoreductases↗

PubMed1992

Evidence for intestinal release of absorbed selenium in a form with high hepatic extraction.

Selenium is readily absorbed from the gastrointestinal tract and utilized for synthesis of selenoproteins. Roles of intestine, liver, and selenoprotein P in this process were evaluated. Rats were given 75Se-selenite by stomach tube, and distribution of 75Se was followed for 3 h. A high portal vein plasma-to-hepatic vein plasma ratio of 75Se 15 min after 75Se administration and earlier uptake by liver than by other tissues indicated avid hepatic extraction of absorbed selenium from portal vein blood. The results of gel filtration of plasma taken 15 min after 75Se administration suggested that the 75Se was in the form of small molecules with some affinity for protein. Immunoprecipitation studies using plasma indicated that 75Se began to appear in selenoprotein P between 15 and 30 min after intragastric administration. To evaluate the role of the liver in the fate of absorbed selenium, rats with portacaval shunts, in which absorbed selenium bypasses the liver, were compared with sham-operated rats. After intragastric administration of selenium, uptake by the liver and incorporation into selenoprotein P were diminished in rats with portacaval shunts but kidney uptake and urinary excretion were increased. This suggests that hepatic extraction of absorbed selenium from portal vein blood decreases its entrance into the systemic circulation. The results of this study indicate that intestine releases absorbed selenium into portal blood in a small-molecule form, designated A-Se, which is highly extracted by the liver. The liver takes up A-Se better than other tissues because of a high extraction capacity and the fact that it is the first organ through which the blood from the intestine passes.

Absorption↗

PubMed2006

High serum selenium and reduced risk of advanced colorectal adenoma in a colorectal cancer early detection program.

BACKGROUND: Epidemiologic and animal studies suggest that selenium may reduce risk of colorectal cancer. However, the epidemiologic data is mainly from relatively small investigations, limiting their interpretation. Although substantial evidence suggests that smoking is a strong effect modifier for other antioxidative nutrients, little is known about smoking-selenium interactions in colorectal tumors. METHODS: We studied the association of serum selenium and advanced colorectal adenoma, a cancer precursor, in 758 cases and 767 sex- and race-matched controls, randomly selected from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cases had at least one verified advanced adenoma (> or = 1 cm or villous elements, or high-grade dysplasia) of the distal colon, and controls had a negative sigmoidoscopy. RESULTS: The multivariable odds ratio (OR) comparing participants in the highest quintile of serum selenium with those in the lowest quintile was 0.76 [95% confidence interval (95% CI), 0.53-1.10; P(trend) = 0.01]. The inverse association between serum selenium and advanced colorectal adenoma was significant among recent smokers (OR, 0.53; 95% CI, 0.27-1.01 for highest versus lowest tertile; P(trend) = 0.008). Serum selenium was unrelated to adenoma risk in nonsmokers and former smokers who quit smoking > or = 10 years ago. CONCLUSION: Selenium may reduce the risk of developing advanced colorectal adenoma, particularly among the high-risk group of recent smokers.

Adenoma↗

PubMed2006

Dietary selenium intake and genetic polymorphisms of the GSTP1 and p53 genes on the risk of esophageal squamous cell carcinoma.

Few studies have assessed potential effect modifications by polymorphisms of susceptibility genes on the association between selenium intake and esophageal squamous cell carcinoma (ESCC). We studied the joint effects of dietary selenium and the GSTP1 and p53 polymorphisms on ESCC risk in a population-based case-control study with 218 ESCC cases and 415 controls in Taixing City, China. Dietary selenium intake was estimated from a food frequency questionnaire with 97 food items. GSTP1 and p53 polymorphisms were detected by RFLP-PCR assays. Logistic regression analyses were done to estimate odds ratios (OR) and 95% confidence intervals (95% CI). Reduced ESCC risk was observed among individuals in the highest quartile of dietary selenium intake (adjusted OR, 0.31; 95% CI, 0.13-0.70) with a dose-dependent gradient (P(trend) = 0.01). The p53 Pro/Pro genotype was associated with increased risk of ESCC compared with the Arg/Arg genotype (adjusted OR, 2.02; 95% CI, 1.19-3.42). When combined with selenium consumption, an obvious increased risk was observed among individuals with the p53 Pro/Pro or GSTP1 Ile/Ile genotype with adjusted ORs of 3.19 (95% CI, 1.74-5.84) and 1.90 (95% CI, 1.03-3.51), respectively. Among smokers and alcohol drinkers, elevation of ESCC risk was more prominent among p53 Pro/Pro individuals who consumed a low level of dietary selenium (adjusted OR, 3.59; 95% CI, 1.49-8.66 for smokers and 6.19; 95% CI, 1.83-20.9 for drinkers). Our study suggests that the effect of dietary selenium on the risk of ESCC may be modulated by tobacco smoking, alcohol drinking, and p53 Pro/Pro and GSTP1 Ile/Ile genotypes.

Aged↗

PubMed2003

Selenium in breast cancer.

AIM: Controversy surrounds the hypothetical relationship between low serum levels of selenium and reduced activity of selenium-dependent enzymes, such as glutathione peroxidase, and an increased risk of cancer in humans. This study investigated serum concentrations of selenium in women with and without breast cancer. METHODS: In this case-control study, we compared serum concentrations of selenium in women with breast cancer (n = 200), healthy women (n = 100), and women with chronic diseases (n = 100). Patients with breast cancer were divided into premenopausal (n = 99) and postmenopausal subjects (n = 101). RESULTS: Mean serum concentrations of selenium were 81.1 microg/l in women with breast cancer and 98.5 microg/l in women with non-tumoral disease (p < 0.001). CONCLUSION: Alterations in serum concentrations of selenium in women with breast cancer appear to be a consequence, rather than a cause of cancer. In accordance with the hypothesis, the findings suggest that very low selenium status could be due to the nature of cancer.

Acute Disease↗

PubMed1980

Selenium in premature infants.

Premature infants have a lower selenium concentration in serum than full-term infants and children. The selenium concentration goes down quickly in infants treated for respiratory distress syndrome without supplementation. One premature infant with bronchopulmonary dysplasia had persistently low concentrations of selenium. Vitamin E supplements did not affect the serum selenium concentration in healthy premature infants. Supplementation with 3 microgram/kg of selenium in parenteral fluids prevented the fall in the concentration seen in other infants not supplemented. Premature infants and especially those treated with oxygen may warrant selenium supplementation to the parenteral nutrition solution. Vitamin E supplements alone are apparently not sufficient to prevent selenium deficiency and potential oxygen toxicity.

Adolescent↗

PubMed1993

Hypercholesterolemia promotes endothelial dysfunction in vitamin E- and selenium-deficient rats.

Abnormal regulation of local vascular tone occurs early in human and experimental atherosclerosis. Impaired endothelium-dependent vascular relaxations mediated by endothelium-derived relaxing factor are an important contributor to these abnormalities. Endothelium-derived relaxing factor is nitric oxide released as such or attached to a carrier molecule. Oxidized lipoproteins impede endothelium-derived relaxing factor-mediated responses in vitro. We designed in vivo experiments to determine whether hypercholesterolemia with and without deficiency of two endogenous lipid antioxidants, vitamin E and selenium, would result in endothelial dysfunction. Vitamin E and selenium deficiencies were induced in a group of hypertension-prone Dahl salt-sensitive rats fed a diet high in cholesterol (4%) but low in NaCl (0.5%) for 18 weeks. Two other groups of Dahl salt-sensitive rats received diets sufficient in vitamin E and selenium but containing either high or normal cholesterol levels (control group). Serum cholesterol levels increased approximately 10-fold in the two groups of rats fed high-cholesterol diets. Systolic blood pressure was 143 +/- 3 mm Hg in high-cholesterol/vitamin E- and selenium-sufficient rats and 142 +/- 5 mm Hg in high-cholesterol/vitamin E- and selenium-deficient rats (P = NS). Mild intimal thickening and occasional mononuclear cell infiltration were observed in both of these groups. Serum vitamin E levels were decreased, whereas serum thiobarbituric acid-reactive substances and exhaled pentane (two indicators of endogenous lipid oxidation) were significantly increased in high-cholesterol/vitamin E- and selenium-deficient rats compared with high-cholesterol/vitamin E- and selenium-sufficient rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1998

Vitamin E combined with selenium inhibits atherosclerosis in hypercholesterolemic rabbits independently of effects on plasma cholesterol concentrations.

Several antioxidants inhibit atherosclerosis. This study investigated the hypothesis that combining vitamin E, a lipophilic antioxidant, with vitamin C, a hydrophilic antioxidant, and/or selenium, a cofactor of peroxidases that detoxify lipid peroxides, would inhibit atherosclerosis more effectively than vitamin E alone. We also considered whether regional variation in inhibition of atherosclerosis by antioxidants would be associated with regional variation in aortic lipophilic antioxidants. Rabbits were fed an atherogenic diet (control) or an atherogenic diet supplemented with vitamin E, vitamins E and C, vitamin E+selenium, vitamins E and C+selenium, or probucol (positive control). Supplements were as follows: vitamin E, 146 IU/d; vitamin C, 791 mg/d; selenium, 22 microg/d; or probucol, 406 mg/d. Vitamin C did not influence atherosclerosis. After 22 weeks of treatment, rank order of aortic atherosclerosis was control>vitamin E (with or without vitamin C)>vitamin E+selenium (with or without vitamin C)>probucol. Antioxidant treatment reduced aortic cholesterol concentrations 21% to 56%, 29% to 86%, and 19% to 75% for the aortic arch, descending thoracic aorta, and abdominal aorta, respectively (P<0.025 to P<0.0003 by ANOVA), with slightly greatly reductions for areas of atherosclerotic lesions. Some treatments reduced plasma cholesterol concentrations, but none altered the distribution of cholesterol among lipoproteins. Corrected for differences in plasma cholesterol concentrations, aortic cholesterol concentrations were reduced up to 72% (P<0.02) by the antioxidant treatments, with equal reductions by vitamin E+selenium and by probucol. Aortic alpha-tocopherol standardized by aortic cholesterol as a measure of aortic lipids was lower in the abdominal aorta than in the aortic arch of rabbits not given alpha-tocopherol and increased relatively more in the abdominal aorta than in the aortic arch with alpha-tocopherol supplementation. The results of this study suggest that vitamin E+ selenium inhibited atherosclerosis as effectively as an equally hypocholesterolemic dose of probucol by a mechanism(s) that is in part independent of effects on plasma and lipoprotein cholesterol concentrations. The tendency for greater efficacy of antioxidant treatments in the abdominal aorta than aortic arch may relate to the lower concentrations of alpha-tocopherol in the abdominal aorta of unsupplemented rabbits.

Animals↗

PubMed1986

Glutathione peroxidase protein. Absence in selenium deficiency states and correlation with enzymatic activity.

Glutathione peroxidase (GSHPx) activity is an indicator of selenium status in selenium-deficient individuals. Utilizing polyclonal monospecific antibodies to purified erythrocyte GSHPx, we were able to determine the relationship between enzymatic activity and protein content. In erythrocytes from a selenium-deficient individual who was treated with selenium, and in HL-60 cells grown in the absence of selenium and then returned to selenium-containing medium, there was a direct relationship between enzymatic activity and protein content. Thus, selenium deficiency results not only in a decrease of GSHPx activity, but also in a decrease of GSHPx protein.

Antibodies, Monoclonal↗

PubMed1992

Selenium deficiency in long-term total parenteral nutrition.

Although selenium is an essential trace element, it is often not routinely added to total parenteral nutrition (TPN) formulations. When selenium is not added, patients are at risk for selenium deficiency. This report describes such a patient. He had several operations for colon cancer, including a massive resection of the small bowel that resulted in a short bowel and a fistula. TPN was started after his last operation. After he was discharged, he had a normal, active lifestyle, except that he limited oral intake to water and an occasional soft drink. After 3 years of almost exclusive nourishment by TPN, he developed whitened nail beds. Investigation for possible trace element deficiency resulted in a finding that he had very low levels of selenium in his blood. He did not have any of the cardiac or skeletal muscle abnormalities that have been associated with selenium deficiency. After supplementation with selenium, his blood levels of selenium rose and the nail bed changes were reversed.

Aged↗

PubMedDate not supplied

Selenium supplementation in low-birthweight premature infants: relationship to trace metals and antioxidant enzymes.

We attempted to study the effect of selenium supplementation upon trace metal metabolism in low-birthweight infants less than 1000 g birthweight. Serum levels of the trace metals copper, zinc, and selenium; and white blood cell glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were measured in conjunction with the trace metals when parenteral nutrition (TPN) was begun (sample A), at the initiation of enteral nutrition (sample B), and when TPN was discontinued (sample C). Two randomly selected groups of infants were evaluated: group S received selenium supplementation (1.34 micrograms/kg per d) in their parenteral nutrition solutions; group C was a control which did not receive selenium supplementation. Selenium levels declined to equally low levels in both groups by sample C, but were significantly higher in group S at sample B. GSH-Px activities demonstrated a significant increase at sample B in group S and then tended to decrease. In group C, GSH-Px tended to increase, then decreased significantly by sample C. Both groups received 20 micrograms/kg per d of copper in TPN, however, serum copper declined significantly at sample B in group S whereas there were no significant changes in group C. There were no significant changes in zinc and SOD levels. There were no significant differences between groups in clinical characteristics or outcome. This study suggests that a dose of supplemental selenium of 1.34 micrograms/kg per d in TPN is inadequate for low-birthweight premature infants. Selenium supplementation may also affect copper metabolism.

Copper↗

PubMed1995

Inhibition of aflatoxin B1-induced cell injury by selenium: an in vitro study.

Dietary selenium is an essential trace element in human nutrition. Selenium has been shown in animal studies to inhibit aflatoxin hepatocarcinogenesis. However, the cellular mechanism responsible for the inhibition has not been thoroughly studied. This study examines the effect of two selenium compounds, namely, sodium selenite and selenium-enriched yeast extract (SeY), on the cytotoxicity, DNA-binding and mutagenicity of aflatoxin B1 (AFB1) in cultured Chinese hamster ovary (CHO) cells. CHO cells, after treatment with 2 micrograms ml-1 selenite or 80 micrograms ml-1 SeY, exhibited increased resistance to AFB1-induced cell killing. At a concentration of 50 micrograms ml-1 AFB1, cell survival, measured by the clonogenicity assay, was increased by 21- and 10-fold in selenite- and SeY-treated cells, respectively. However, selenium treatment did not appear to affect AFB1-DNA binding. Similarly, no effect was observed on AFB1 mutagenicity, as determined by the hypoxanthine-guanine phosphoribosyl transferase (HPRT) gene mutation assay. The results showed that selenium could effectively protect cells from AFB1 cytotoxicity in cultured cells but had no effect on AFB1-DNA adduct formation or mutagenesis. It is suggested that there are multiple pathways of AFB1 toxicity and that selenium can modulate AFB1-induced cell killing independent of its genotoxicity.

Aflatoxin B1↗

PubMed2004

Cross-species global and subset gene expression profiling identifies genes involved in prostate cancer response to selenium.

BACKGROUND: Gene expression technologies have the ability to generate vast amounts of data, yet there often resides only limited resources for subsequent validation studies. This necessitates the ability to perform sorting and prioritization of the output data. Previously described methodologies have used functional pathways or transcriptional regulatory grouping to sort genes for further study. In this paper we demonstrate a comparative genomics based method to leverage data from animal models to prioritize genes for validation. This approach allows one to develop a disease-based focus for the prioritization of gene data, a process that is essential for systems that lack significant functional pathway data yet have defined animal models. This method is made possible through the use of highly controlled spotted cDNA slide production and the use of comparative bioinformatics databases without the use of cross-species slide hybridizations. RESULTS: Using gene expression profiling we have demonstrated a similar whole transcriptome gene expression patterns in prostate cancer cells from human and rat prostate cancer cell lines both at baseline expression levels and after treatment with physiologic concentrations of the proposed chemopreventive agent Selenium. Using both the human PC3 and rat PAII prostate cancer cell lines have gone on to identify a subset of one hundred and fifty-four genes that demonstrate a similar level of differential expression to Selenium treatment in both species. Further analysis and data mining for two genes, the Insulin like Growth Factor Binding protein 3, and Retinoic X Receptor alpha, demonstrates an association with prostate cancer, functional pathway links, and protein-protein interactions that make these genes prime candidates for explaining the mechanism of Selenium's chemopreventive effect in prostate cancer. These genes are subsequently validated by western blots showing Selenium based induction and using tissue microarrays to demonstrate a significant association between downregulated protein expression and tumorigenesis, a process that is the reverse of what is seen in the presence of Selenium. CONCLUSIONS: Thus the outlined process demonstrates similar baseline and selenium induced gene expression profiles between rat and human prostate cancers, and provides a method for identifying testable functional pathways for the action of Selenium's chemopreventive properties in prostate cancer.

Adenocarcinoma↗

PubMed1978

Modification of methylmercury toxicity and metabolism by selenium and vitamin E: possible mechanisms.

Selenium and vitamin E exert powerful effects in reducing acute or chronic methylmercury toxicity. Levels of selenium normally found in foods (below 1 ppm) delay the onset of toxic signs caused by much higher levels of methylmercury. Tissue levels of mercury in selenium-supplemented animals equal or exceed those found in animals given methylmercury alone. Selenium does not appear to act by simply modifying intake, absorption, excretion, or distribution of methylmercury, and direct effects of both selenium and vitamin E have been observed in vitro when methylmercury was added to cultured nervous tissue cells. The only established functions for selenium and vitamin E in animals are related to the prevention of oxidative damage in tissues. To encompass the protective effects of selenium and vitamin E and to explain other toxicological aspects of methylmercury and other alkylmetals, a new hypothesis is proposed: The toxicity of the alkylmetals is not caused soley by the intact molecule, but also involves free radicals formed by homolytic fission of the carbon-metal bond.

Animals↗

PubMed1989

Studies on serum selenium and tocopherol in white muscle disease of foal.

In order to clarify the cause of white muscle disease (W.M.D.) in foals, tocopherol and selenium concentrations in serum and glutathione peroxidase activities in blood were measured. Examination was made on the samples from horses affected with W.M.D., the foal kept with them in the same stable, the foals kept in the stables without affected foals, and respective mares. The heavy-breed horses in Fukuoka prefecture and Tokachi district were also examined for comparison. Serum tocopherol levels of these foals were normal because after intake of colostrum. Mares of affected foals showed lower tocopherol levels than other examined mares (p less than 0.01). Serum selenium levels of all foals were below 65 ppb, showing deficient levels. The mares of affected foals had lower selenium levels than other mares (p less than 0.01). There was a good correlation between serum selenium concentration and blood glutathione peroxidase activity (r = 0.81). Selenium levels in the liver of affected foals were lower than the foals which succumbed with other diseases. Diet supplied in the stables with affected foals showed low alpha-tocopherol and selenium contents. These findings suggest that W.M.D. in foals is attributed to nutritional muscular dystrophy caused by tocopherol and selenium deficiency of their mares in late gestation period.

Animals↗

PubMed2004

Plasma selenium decrease during pregnancy is associated with glucose intolerance.

There is an increased requirement for selenium during pregnancy, presumably for fetal growth, which manifests as decreasing maternal blood and tissue selenium concentrations. These decreases are greater in pregnant women with gestational or preexisting diabetes. We measured selenium status and glucose tolerance between wk 12 and 34 of gestation in 22 pregnant women. We found that the increase in blood glucose in response to an oral glucose challenge at 12 wk gestation and the increase in fasting glucose during pregnancy were inversely correlated with plasma selenium concentration. Women with lower plasma glutathione peroxidase activities during pregnancy also tended to have higher fasting glucose levels. These inverse relationships between selenium status and glucose tolerance are consistent with earlier observations that suggest a link between selenium and glucose metabolism. The observation that changes in serum glucose were not accompanied by changes in insulin suggests that selenium may affect glucose metabolism downstream from insulin, or through independent energy regulatory pathways such as thyroid hormone.

Adult↗

PubMed2006

Selenium and zinc in patients with acute and chronic uveitis.

Patients with chronic inflammation often show decreased serum levels of trace elements. This study aimed to investigate serum levels of selenium and zinc in patients with uveitis. Twenty-four patients (13 female, 11 male) with a mean age of 40.6 +/- 15.5 yr were included in this study. According to their underlying disease, they were divided into acute (n = 13) or chronic (n = 11) uveitis. Selenium and zinc determination was performed by atomic absorption spectroscopy in EDTA blood samples. Patients with acute or first-time uveitis showed selenium and zinc concentrations within the normal range. In contrast to this, patients with chronic recurrent uveitis tend to result in decreased selenium and zinc levels. Especially selenium showed a remarkable reduction in serum concentration below the normal range. Furthermore, there was a tendency to decreased trace element concentrations with increasing age. A sex dependency could not been found. Especially patients with chronic, recurring uveitis show remarkable decreased selenium concentration in the EDTA-blood. Further studies should investigate possible positive effects of therapeutic selenium and zinc supplementation in patients with chronic, recurrent uveitis.

Acute Disease↗