Disease relevance of SELENOCYANATE ION

• The incidence of hepatic necrosis was elevated in BOP-treated hamsters fed the unsupplemented diet, and that of biliary cystic adenomas was highest in the group fed 0.1 ppm Se before and after BOP treatment [1].
• Ni and Se x-ray absorption spectroscopic studies of the [NiFeSe]hydrogenases from Desulfovibrio baculatus are described [2].
• Four groups of mice [Se-deficient or -adequate GPX1 knockout and wild-type (WT)] were injected (i.p.) with 50 mg paraquat/kg body weight and tissues were collected 0, 0.5, 1, 2, 3, or 4 h after the injection [3].
• The increase in TR activity produced by 1 microM Se compared to medium with no added selenium was: for MCF-7 breast cancer cells, 37-fold; for HT-29 colon cancer cells, 19-fold; and for A549 lung cancer cells, 8-fold [4].
• The acceptor substrate specificity suggested that both the Se and the H gene dependent alpha-2-L-fucosyltransferases are increased in carcinomas [5].

Psychiatry related information on SELENOCYANATE ION

• Concentrations of 13 trace elements (Ag, Br, Co, Cr, Cs, Fe, Hg, K, Na, Rb, Sc, Se, Zn) in isolated subcellular fractions (whole brain, nuclei, mitochondria, microsomes) of temporal lobe from autopsied Alzheimer's disease (AD) patients and normal controls were determined utilizing instrumental neutron activation analysis [6].
• In OPF, Se-deficient females exhibited less locomotor activity, more defecation, and less entry to the center square areas than did the control females [7].
• This could be attributed to differences in Se content of soil and/or differences in dietary habits of the populations [8].
• Because Cu, Se, and Zn are involved in immune and antioxidative defense mechanisms and tissue repair, deficiencies might aggravate complications classically observed with burns [9].
• The effect of reaction time, pH, and competitive anions at different concentrations on the adsorption of both As and Se species were investigated [10].

High impact information on SELENOCYANATE ION

• Rapamycin-mediated inactivation of TIF-IA is caused by hypophosphorylation of Se 44 (S44) and hyperphosphorylation of Se 199 (S199) [11].
• As a measure of Se status, glutathione peroxidase (GSHPX) activities were determined in plasma, erythrocytes, and liver [1].
• In studies designed to determine the influence of dietary Se on pancreatic carcinogenesis, Syrian golden hamsters were fed unsupplemented torula yeast diet or diet supplemented with 0.1 or 5.0 ppm Se, from sodium selenite, starting at 4 weeks of age until the termination of the study [1].
• Pancreatic ductular adenoma yields were highest in all male groups given diets of 0.1 ppm Se before BOP administration, irrespective of the Se level after BOP was fed [1].
• In the hormonally stimulated mammary gland, increasing dietary Se to 2.0 ppm increased GSH-Px activity threefold and decreased mammary-gland-membrane-localized lipid peroxidation by 16% [12].

Chemical compound and disease context of SELENOCYANATE ION

• Vitamin E deficiency enhanced the antimalarial action of QHS against Plasmodium yoelii, both in terms of decreased parasitemia and improved survival but Se deficiency did not [13].
• The marked elevation of blood pressure at the lowest levels of plasma ascorbic acid and serum Se concentrations supports the hypothesis that antioxidants play a role in the etiology of hypertension [14].
• Galactose-1-P uridylyltransferase purified from Escherichia coli cells grown in enriched medium contains approximately 1.2 mol of tightly bound zinc/mol of subunits as well as variable amounts of iron, up to 0.7 mol/mol of subunits, and no detectable Ca, Cd, Cu, Mo, Ni, Co, Mn, As, Pb, or Se [15].
• Serotype K1 Capsule, Rather than magA Per Se, Is Really the Virulence Factor in Klebsiella pneumoniae Strains That Cause Primary Pyogenic Liver Abscess [16].
• A 3 x 3 factorial experimental design was used to examine the acute effects of DMH treatment (0, 10 and 20 mg/kg body weight) interacting with dietary Se levels (less than 0.02, 0.1 and 0.5 mg/kg diet as sodium selenite) [17].

Biological context of SELENOCYANATE ION

• The marginal decrease in lipid peroxidation found in the mammary glands exposed to 2.0 ppm Se could not explain the inhibitory effect of Se on tumorigenesis [12].
• Here we report the spatial distribution and chemical forms of selenium in Astragalus bisulcatus (two-grooved poison or milk vetch), a plant capable of accumulating up to 0.65% of its shoot dry biomass as Se in its natural habitat [18].
• Recently, the FUT2 and a pseudogene have been isolated, and an Se enzyme-deficient allele (se) caused by a nonsense mutation (G428A, se1) in Caucasians has also been reported [19].
• Based on a lod score of 12.9 at 1% recombination units and the existence of two different acceptors for the biosynthesis of the H antigen, a new genetic model is proposed in which H and Se would be two closely linked structural genes coding for two different 2-alpha-L-fucosyltransferases [20].
• This conclusion correlates well with the finding that H and Se genes are closely linked and might have derived by gene duplication in the course of evolution [21].

Anatomical context of SELENOCYANATE ION

• Possible mechanisms for the inhibitory effect of selenium on mouse mammary gland tumorigenesis were evaluated in two different mouse models, in 7,12-dimethylbenz[a]anthracene [(DMBA) CAS:57-97-6]treated and hormonally stimulated mammary glands with two dietary levels of Se (0.2 and 2.0 ppm) [12].
• Human leukemia K562 cells (capable of expressing PHGPX but not GPX) exhibited 5- to 10-fold lower PHGPX activity under Se-deficient relative to Se-sufficient conditions [22].
• Activity of the human blood group ABO, Se, H, Le, and X gene-encoded glycosyltransferases in normal and malignant bladder urothelium [23].
• Utilizing the HL-60 human promyelocytic leukemia cell line cultured in defined medium, we examined the quantitative and temporal relationships between Se supply and the activity of the selenoenzyme glutathione peroxidase, as well as the effects of selenium deficiency on phagocytic function [24].
• Proliferation of bovine endothelial cells was enhanced by 5 X 10(-7) M Se [25].

Associations of SELENOCYANATE ION with other chemical compounds

• Disruption of the cysK gene prevented synthesis of free cysteine and selenocysteine from inorganic S and Se precursors [26].
• Whereas the ratios of NADPH/NADP and NADH/NAD in lung were reduced by 50-70% only 0.5 h after the injection in all groups, these two ratios in liver of the Se-adequate WT were significantly higher than those of the three GPX1 knockout or deficient groups 2-4 h after the injection [3].
• Glutathione peroxidase activity depended on the medium Se concentration up to 2.6 X 10(-8) M (sodium selenate, 5 ng/ml), above which a plateau occurred [24].
• Se-deficient mature HL-60 cells stimulated with phorbol myristate acetate released 2.3-fold more H2O2 than Se-replete cells and only slightly (not significantly) less O2 [24].
• Solid-state NMR analysis on wurtzite 2-nm hexadecylamine-capped CdSe nanocrystals (CdSe-HDA) provides evidence of discrete nanoparticle reconstruction within the Se sublattice of the nanomaterial [27].

Gene context of SELENOCYANATE ION

• Therefore, the low level of GPX1 activity in the Se-deficient mice can exert a potent role in defending against liver aponecrosis induced by moderate oxidative stress [28].
• Inhibition by hypericin in the dark was demonstrated for purified CuZnSOD, Se-dependent glutathione peroxidase, glutathione S-transferase, and glutathione reductase activities in vitro [29].
• Surprisingly, we found that GPX1 transcripts in Se deficiency are moderately abundant and similar in abundance to GAPDH and other selenoprotein mRNAs; Se supplementation increases GPX1 mRNA so that it is 30-fold higher than GAPDH mRNA [30].
• The mRNA levels for all selenoproteins in blood were comparable to levels in the major organs, and decreases in blood and liver GPX1 mRNA levels in Se deficiency were similar, supporting potential use of whole blood for assessing Se status using molecular biology markers [31].
• Liver catalase activity increased at least 72% during deficiencies of Se and vitamin E. In summary, GSH-Px did not respond to increased oxidative stress associated with elevated dietary iron except for the non Se GSH-Px which accounts for a relatively small amount of total activity in liver [32].

Analytical, diagnostic and therapeutic context of SELENOCYANATE ION

• A radioimmunoassay specific for the H type 1 antigenic determinant demonstrated that the H type 1 antigen is under the strict control of the Se gene in both serum and saliva [33].
• When fed chronically, the profile of Se accumulation in various tissues was very comparable after treatment with either GGMSC or MSC [34].
• The multi-isotopic (including non-metals such as S, P, or Se) detection capability, high sensitivity, tolerance to matrix, and large linearity range regardless of the chemical environment of an analyte make ICP MS a valuable complementary technique to electrospray MS and MALDI MS [35].
• The present study was designed to examine the in vivo responses to GGMSC or MSC using a variety of biochemical and biological end points, including (a) urinary Se excretion as a function of bolus dose; (b) tissue Se accumulation profile; (c) anticancer efficacy; and (d) gene expression changes as determined by cDNA array analysis [34].
• These data provide the first example of crystallization of a substrate-reduced form of a Se- and Mo-containing enzyme [36].

References