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PubMed2004

Cloning and heterologous expression of a Methanococcus vannielii gene encoding a selenium-binding protein.

The activation and incorporation of selenium into selenocysteine containing selenoproteins has been well established in an Escherichia coli model system but there is little specific information concerning the transport and intracellular trafficking of selenium in biological systems in general. A selenium transport role is a possible function of a novel 42 kDa selenium-binding protein that recently was purified from Methanococcus vannielii. The gene encoding a monomer of this protein (Sbp) has been cloned, sequenced and heterologously expressed in E. coli. The 8.8 kDa gene product contains 81 amino acids. The recombinant Sbp (rSbp) protein was shown to bind selenium from added selenite. The bound selenium appeared predominantly in dimeric and tetrameric forms of the protein. The gene encoding Sbp occurs in an operon that contains a carbonic anhydrase gene and selenocysteine-containing formate dehydrogenase genes, suggesting possible roles in selenium-dependent formate metabolism.

Amino Acid Sequence↗
PubMed1981

Properties of the mercury and selenium complex formed in rat plasma in vivo.

Properties of the mercury and selenium complex (Hg-Se Complex) produced in plasma after the simultaneous injection of mercuric chloride and sodium selenite were investigated by means of pronase digestion and isoelectric focusing. When the gel chromatographic fraction containing the HG-Se complex was digested with Pronase E and chromatographed on a Sephadex G-200 column, the resulting derived proteins contained no mercury and very low percentage of selenium. Most of mercury and selenium in the digest of the Hg-Se complex remained at the top of column, but the content of proteins (derived proteins) found at the same site of column was only trace amount. In contrast, the derived proteins obtained from proteins containing mercury or selenium in serum by the same digestion contained mercury and high percentage of selenium respectively. These results indicated that the Hg-Se complex in plasma did not contain protein as a component. When the isoelectric focusing of the serum containing the Hg-Se complex was carried out, the peak containing both mercury and selenium was present in the position of pH2 and pH4. The former peak was independent of the serum proteins, the latter peak overlapped the distribution of that. Similar behavior of mercury and selenium was observed in the isoelectric focusing of the mercuric selenide colloid dispersed in the solution containing bovine serum albumin. The properties of the Hg-Se complex in these studies supported the hypothesis that it is a mercuric selenide colloid.

Animals↗
PubMed2004

Selenium metabolites in urine: a critical overview of past work and current status.

BACKGROUND: Selenium is an essential trace element that also elicits toxic effects at modest intakes. Investigations of selenium metabolites in urine can help our understanding of the transformations taking place in the body that produce these beneficial and detrimental effects. There is, however, considerable discord in the scientific literature regarding the selenium metabolites thought to play important roles in these biotransformation processes. APPROACH: We critically assessed the published reports on selenium urinary metabolites, from the first report in 1969 to the present, in terms of the rigor of the data on which structures have been proposed. CONTENT: We present and discuss data from approximately 60 publications reporting a total of 16 identified selenium metabolites in urine of humans or rats, a good model for human selenium metabolism. We assessed the analytical methods used and the validity of the ensuing structural assignments. SUMMARY: Many of the studies of selenium metabolites in urine appear to have assigned incorrect structures to the compounds. The long-held view that trimethylselenonium ion is a major human urinary metabolite appears unjustified. On the other hand, recent work describing selenosugars as major urinary metabolites looks sound and provides a firm basis for future studies.

Animals↗
PubMed1993

Renal retention of selenium after administration of trimethylselenide.

Renal retention of selenium after administration of trimethylselenonium iodide (TMSeI) was studied in vivo in male and female rats during sexual maturation. The selenium level in the kidneys was found to be significantly higher in male rats than in females during the first hour after intravenous (i.v.) administration of TMSeI. The sex-linked difference, manifested already in 21-day old animals, increased markedly during the following four weeks of postnatal life. It was shown that this process may be accelerated by previously increased selenium intake. The sex-linked difference in renal retention of selenium was observed after administration of TMSeI in a wide range of doses: 0.002-10.0 mumol per animal. The size of the applied dose did not affect significantly the kinetic patterns of selenium in the kidneys during the first hour after i.v. injection. The results suggest the existence of a sex-dependent mechanism in the kidneys which may control the rate of excretion of trimethylselenonium ions in urine both under conditions of normal selenium intake and selenium intoxication.

Aging↗
PubMedDate not supplied

[Selenium deficiency in patients with cardiovascular diseases and its correction with the drug "selena"].

Blood selenium concentrations, erythrocytic glutathione peroxidase (GPO) activity, and plasma lipid peroxides were investigated in patients with ischemic heart disease (IHD) and dilated cardiomyopathy (DCMP). Patients with IHD and DCMP displayed depressed activity of GPO with activation of lipid peroxides associated with lower blood selenium. The daily intake of 300 micrograms of selenium from Selena during a month treatment augmented selenium concentrations by 71% in IHD and DCMP patients. This augmentation showed an inverse correlation with primary plasma selenium concentrations. Plasma malonic dialdehyde levels decreased by 17%. The findings suggest that selenium is involved in the pathogenesis of DCMP and IHD, which may be a ground for selecting patients with selenium deficiency for its correction with Selena.

Adult↗
PubMed1997

Selenium is required for normal upregulation of myelin genes in differentiating oligodendrocytes.

The purpose of this study was to characterize the selenium requirement for the normal differentiation of oligodendrocyte lineage cells. In primary mixed glial cultures prepared from newborn rat brains, the overall growth of cultures, as seen from the total RNA yield, was not significantly affected by selenium. However, 30 nM selenium was required for the normal upregulation the proteolipid protein, basic protein, and myelin-associated glycoprotein gene expression assessed by Northern blot analysis. Selenium deprivation during initial, rapid phase of the gene upregulation irreversibly suppressed the genes, indicating the existence of a critical period in oligodendrocyte differentiation. In purified oligodendrocyte cultures prepared by mechanical dislodging of progenitor (O-2A) cells from mixed glial cultures, total cell number and total RNA yield were virtually unaffected by selenium deprivation; however, the developmental upregulation of the myelin genes was profoundly attenuated. Immunocytochemical analysis confirmed the suppressive effect of selenium deficiency on the differentiation of oligodendrocyte lineage cells, as seen from a significant decrease in the population of GalC+ and O4+ cells. Because the number of GC+ cells was more reduced than the number of O4+ cells, the results indicate that selenium deficiency may specifically inhibit the progression from immature to mature oligodendrocytes.

Animals↗
PubMed1983

Selenium and glutathione peroxidase levels in patients with epidermoid carcinoma of the oral cavity and oropharynx.

Selenium ingestion may inhibit carcinogenesis. Epidemiologic studies have shown that age-adjusted death rates for cancer at most head and neck sites are lower in states where the soil and forage crops contain higher levels of selenium. The mode of action is incompletely understood, but may be mediated through an increase in the activity of the selenium dependent, antioxidant enzyme glutathione peroxidase (GSH-Px). The authors studied blood selenium levels and blood and tissue GSH-Px activities in 50 patients with untreated cancer of the oral cavity and oropharynx. Mean erythrocyte selenium and glutathione peroxidase were significantly depressed when compared to age-matched controls. Mean plasma selenium, on the other hand, was significantly elevated in the cancer patient group. Data from subsets within the cancer patient group were also discussed. GSH-Px activity did not differ in tumor and adjacent normal tissue. The concept of chemoprevention of carcinogenesis with inhibitory chemical compounds is particularly apropos to head and neck cancer control. Further work is indicated to determine if ingestion of supplemental selenium corrects the abnormalities identified here, and what affect, if any, this would have on the development and behavior of squamous cell cancers in the upper aerodigestive tract.

Aged↗
PubMed1987

Plasma selenium levels in patients with advanced upper gastrointestinal cancer.

Plasma selenium levels were determined at various intervals during hospitalization of 71 patients with upper gastrointestinal and other malignancies. These patients often require frequent nutritional as well as surgical or medical intervention. Attempts were made to identify, evaluate, and compensate for numerous confounding variables at each of the 374 plasma selenium determinations. Selenium levels in stable patients who were neither receiving aggressive antineoplastic therapy, nor septic, nor taking corticosteroids and who had no clinically significant metabolic imbalance were then separately analyzed. In 55 stable patients selenium levels were 28% lower than those found in 20 normal controls (mean 61.8 micrograms/L, P less than 0.0005). An analysis of all the readings showed that selenium levels were substantially decreased by recent radiotherapy or sepsis, by regional tumor spread and increased tumor burden, and by intravenous and/or enteral hyperalimentation and intravenous lipids. In contrast to these findings, levels were relatively higher in patients with an adequate oral diet or with a lesser tumor burden. The comparison between selenium levels in stable and in aggressively treated or septic patients supports the importance of the relationship of nutrition to selenium levels in cancer patients.

Adult↗
PubMed2004

Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat.

Selenium deficiency causes oxidative stress and impairs steroidogenesis in vitro. Leptin is closely related to the hypothalamo-pituitary-adrenal (HPA) axis. Leptin inhibits the HPA axis at the central level while corticosteroids have been shown to stimulate leptin secretion in most studies. We hypothesized that oxidative stress impairs adrenal steroidogenesis and decreases leptin production in vivo. The goal of this study was to investigate in rats the effects of selenium deficiency and oxidative stress on adrenal function and on leptin concentrations. Weanling rats were fed a selenium-deficient (Se-) or selenium-sufficient (Se+) diet for 4-10 weeks. Selenium deficiency caused a marked decrease in liver (> or = 99%) and adrenal (> or = 81%) glutathione peroxidase (GPx) activities. Selenium deficiency did not affect basal and short-term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. In contrast, after long-term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. Plasma leptin concentrations were 50% lower in Se- compared to Se+ animals following long-term ACTH. Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations.

Adrenal Glands↗
PubMed2006

Dietary selenium intake, aldehyde dehydrogenase-2 and X-ray repair cross-complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma.

BACKGROUND: To the authors' knowledge, few studies have been conducted to date regarding dietary selenium and the potential gene-nutrient interactions with single-nucleotide polymorphisms (SNPs) in different pathways on the risk of esophageal cancer. METHODS: The authors investigated the role of dietary selenium intake and its interplay with SNPs of the ALDH2 (glutamic acid [Glu] 487 lysine [Lys]) and the X-ray repair cross-complementing 1 (XRCC1) (arginine [Arg] 399 glutamine [Gln]) genes on the risk of esophageal squamous cell carcinoma (ESCC) in a population-based, case-control study in China. In total, 218 patients with ESCC and 415 healthy population control participants were interviewed. Dietary selenium intake was estimated from a food frequency questionnaire with 97 food items. ALDH2 and XRCC1 polymorphisms were detected with a polymerase chain reaction-restriction fragment length polymorphism assay. RESULTS: The adjusted odds ratio (OR) for the highest quintile of dietary selenium intake, compared with the lowest quintile of intake, was 0.48 (95% confidence interval [95% CI], 0.25-0.89), with a strong dose-response relation (P for trend, <.01). The ALDH2 Lys and XRCC1 Gln variant alleles were associated with an increased risk of ESCC with adjusted ORs of 1.91 (95% CI, 0.96-3.80) and 1.67 (95% CI, 1.08-2.59), respectively. An elevation of the risk for ESCC was pronounced most among carriers of ALDH2 Lys/Lys and XRCC1 399Gln/Gln or Gln/Arg who consumed a low level of dietary selenium (adjusted OR, 4.16; 95% CI, 1.14-15.12). CONCLUSIONS: To the authors' knowledge, this is the first in-depth study to suggest that genetic susceptibility may modify the association between selenium intake and the risk of ESCC. The findings indicated that individuals with low dietary selenium intake and ALDH2 Lys/Lys and XRCC1 399Gln/Gln or Gln/Arg genotypes were associated with an increased ESCC risk, especially in the presence of exposure to tobacco and alcohol carcinogens.

Aged↗
PubMed1998

Plasma selenium in patients with cirrhosis.

Plasma selenium concentration is decreased in patients with cirrhosis and, based on this finding, it has been suggested that patients with cirrhosis are selenium deficient. We measured plasma selenium concentration and the two plasma selenoproteins, glutathione peroxidase (GSHPx-3) and selenoprotein P, in the plasma of patients with cirrhosis of Child classes A, B, and C and in control subjects. Plasma selenium declined in proportion to the severity of the cirrhotic condition, as indicated by the Child class. Selenoprotein P, which originates largely in the liver, declined in a similar manner. Plasma glutathione peroxidase activity increased, and GSHPx-3 originates in the kidney. Selenium in the non-selenoprotein pool, shown by others to be largely selenomethionine in albumin, declined. Thus, although plasma selenium is decreased in patients with cirrhosis, the increase in plasma glutathione peroxidase activity, which occurs in them, suggests that patients with cirrhosis do not have selenium deficiency.

Adult↗
PubMed2006

Monomethylated selenium inhibits growth of LNCaP human prostate cancer xenograft accompanied by a decrease in the expression of androgen receptor and prostate-specific antigen (PSA).

OBJECTIVES: Epidemiological studies and prevention trials suggest selenium is a promising preventive agent for prostate cancer. Selenium-containing compounds inhibited the growth of prostate cancer cell lines including androgen sensitive LNCaP and androgen insensitive DU145 and PC3 cells in vitro. Previous study revealed a novel mechanism of selenium action in which selenium (methylseleninic acid (MSA)) markedly reduced androgen receptor (AR) signaling in prostate cancer cells, suggesting that selenium might act as an antiandrogen, which could serve as a therapeutic agent for prostate cancer. In this study, we tested whether selenium (methylselenocysteine (MSC)) affects tumor growth of human prostate cancer cells by targeting AR signaling in vivo. METHODS: Prostate tumor xenografts were established in nude mice by co-inoculating LNCaP cells with Matrigel. The mice-bearing tumors were treated with or without MSC (100 microg/mouse/day) via intraperitoneal injection for 2 weeks. The effect of MSC on tumor growth, AR, and prostate-specific antigen (PSA) expression was examined. RESULTS: Methylselenocysteine (MSC) significantly inhibited LNCaP tumor growth (P < 0.05). AR expression in tumor tissues and serum PSA levels were considerably decreased in MSC-treated mice compared to the vehicle controls. CONCLUSIONS: Pharmacological dose of MSC inhibits the growth of LNCaP human prostate cancer in vivo accompanied by a decrease in the expression of AR and PSA. These findings suggest that selenium (MSC) can serve as a therapeutic agent aimed at disruption of AR signaling for prostate cancer.

Animals↗
PubMed1994

Regulation of glutathione S-transferase gene expression and activity by dietary selenium.

To determine selenium's effects on glutathione S-transferase gene expression and enzyme activity, weanling rats were fed a selenium-deficient diet, or the same diet supplemented with 0.1 (control) or 2.0 mg selenium/kg diet as sodium selenite, for 91 days. Consumption of either the selenium-deficient or high selenium diet increased activity of glutathione S-transferase, measured with 1-chloro-2,4-dinitrobenzene as substrate, compared to the control diet. Transcription of genes for glutathione S-transferase subunits was unaffected by selenium intake. Steady state levels of mRNA for glutathione S-transferase subunits were affected variably by changes in selenium intake, depending upon the tissue and subunit examined. These results suggest that the biological effects of selenium may be due in part to its regulation of gene expression for glutathione S-transferase family enzymes.

Animals↗
PubMed1993

Effect of vitamin B12 status on selenium methylation and toxicity in rats: in vivo and in vitro studies.

Animals are known to convert inorganic selenium to less toxic methylated compounds such as dimethylselenide (DMSe) and trimethylselenonium (TMSe). This study investigated the role of vitamin B12, a cofactor of methionine synthetase, in selenium methylation in the rat. Vitamin B12-depleted rats expired 16% of dosed 75Se-selenite as DMSe compared to 45% for control rats and excreted less TMSe in the urine (6.1% of dose) than control (9% of dose) rats. At the same time, higher (p < 0.05) tissue (liver, kidney, muscle) selenium levels and lower (p < 0.05) blood selenium levels were found in vitamin B12-deficient rats. Primary hepatocytes from vitamin B12-deficient rats volatilized 15% of selenite in incubation medium in 5 hr as compared to 49% in hepatocytes from control rats. Hepatocytes from vitamin B12-deficient rats were less resistant to selenite toxicity. In vitro methylation of selenium with liver extract from vitamin B12-deficient rats showed one-third to one-half the rate of volatilization of selenium as compared to control rats. S-adenosylmethionine was required for this reaction. These results show that vitamin B12 deficiency significantly decreases the ability of rats to methylate selenium.

Animals↗
PubMed1986

Mechanisms of selenium inhibition of tumorigenesis.

Numerous experiments have demonstrated that selenium supplementation to the diet at modest and nontoxic levels is an effective inhibitor of mammary tumorigenesis in mice and rats. In mice, selenium is most effective during the early stages of tumorigenesis, in particular the events surrounding the induction and expression of the preneoplastic transformation. Whereas selenium is an effective chemopreventive agent, there is little data to support its role as an effective therapeutic agent. The mechanisms of selenium-mediated inhibition of tumorigenesis have not been established. However, the available data suggest that selenium does not act by way of the principal selenoprotein in the cell, glutathione peroxidase, nor does selenium inhibit lipid peroxidation. A number of different mechanisms to explain the inhibitory effects of selenium are discussed; however, definitive answers await further experiments.

Animals↗
PubMedDate not supplied

Effects of adriamycin on chronic cardiotoxicity in selenium-deficient rats.

Adriamycin (doxorubicin) is an antineoplastic drug used to treat various cancers; however, its chronic use is unfortunately accompanied by cardiotoxicity. This toxicity can be reduced by antioxidant agents such as selenium, and it is particularly interesting that cancer patients are usually deficient in this trace element, which suggests that its supplementation could contribute to beneficial treatment. We have examined the effect of adriamycin on chronic cardiotoxicity in 6-week selenium deficiency in rats. Selenium-deficient rats showed a considerable reduction of selenium levels and of selenium-containing glutathione peroxidase. Cardiac lipid peroxides increased slightly in the deficient rats, whereas plasma and heart lipid peroxides increased markedly in adriamycin-treated rats. This increase was greatly accentuated in selenium deficiency. These results suggest that free radical mechanism may be contributing to adriamycin toxicity, and above all show the importance of balancing the selenium levels in adriamycin-treated subjects to limit its harmful myocardial action. A decrease in adriamycin cardiotoxicity with no concomitant decrease in its antineoplastic activity would be of considerable value by improving the therapeutic benefit of the drug.

Animals↗
PubMed1993

Modulation of procainamide toxicity by selenium-enriched yeast in rats.

Free radical processes are proposed to play a crucial role in the development of procainamide adverse effects. Therefore, selenium, as a potent antioxidant, may modified procainamide toxicity. To test this hypothesis plasma and liver thiobarbituric acid-reacting substances (TBARS), plasma antioxidant activity (AOA), erythrocyte and liver superoxide dismutase (SOD), catalase, as well as selenium-dependent glutathione peroxidase (Se-GPX) were determined in the following four groups of rats: selenium-treated (Se), procainamide-treated (P), procainamide and selenium-treated (P + Se), and control (C). Morphological studies of leukocytes [tested for lupus erythematosus (LE) cells] and liver were also made. Atypical, i.e. enlarged and swollen, leukocytes resulting from procainamide and selenium treatment were observed. These changes were found in four out of five rats in the Se group, eight out of ten in the P group, and in seven out of ten in the P + Se group. LE-like cells were observed in two rats in the P + Se group. A statistically significant decrease in plasma and liver TBARS by 20% and 36%, respectively, increased activity of SOD by 20%, catalase by 48% and Se-GPX by 15% in erythrocytes, and decreased activity of liver SOD by 17% and catalase by 22% were found in the P + Se group as compared to the P group. These results indicated that selenium exerted antioxidant effects on the procainamide-treated rats. However, selenium did not prevent the development of disturbances in leukocyte morphology, on the contrary, it possibly promoted the conversion of leukocytes to LE cells.

Animals↗
PubMed1996

Effect of selenium on 1,2-dimethylhydrazine-induced intestinal cancer in rats.

PURPOSE: This study was designed to determine the cancer prevention and therapeutic effects of selenium on rats treated with 1,2-dimethylhydrazine (DMH). METHODS: One hundred sixty Spraque-Dawley male rats were divided into seven groups and received 20 mg/kg/week DMH, subcutaneously for 20 weeks. Two different dosages of selenium (8 and 4 ppm) were administered to the rats through drinking water during DMH treatment (B and C groups) or one month before and during DMH treatment (D and E groups). The rats of Groups A (control group), B, C, D, and E were killed immediately after the last DMH injection. The incidence of intestinal cancer in each group was compared. Eight ppm selenium was also administered to rats after DMH treatment (Group F), and survival times were observed and compared with Group G (treated with DMH only). RESULTS: Rats of Groups B and D received 8 ppm selenium and had a significantly decreased incidence of intestinal cancer (from 65.8 percent (Group A) to 33.3 percent (Group B) and 27.8 percent (Group D); P = 0.0225 and 0.0038). Rats receiving 4 ppm selenium had a relatively decreased incidence of intestinal cancer (from 65.8 percent (Group A) to 44.4 percent (Group C) and 47.1 percent (Group E) but P > 0.05). Survival time of Groups F and G showed no difference. CONCLUSIONS: Eight ppm selenium provided via drinking water has a significant intestinal cancer prevention effect in the presence of a high dose of DMH (20 mg/kg x 20 weeks), and the cancer therapeutic effect of selenium is doubtful in this animal model.

1,2-Dimethylhydrazine↗