Disease relevance of SODIUM SELENITE

• Oxidation of elemental selenium to selenite by Bacillus megaterium [1].
• Mature irreversible cataracts formed approximately 6 days after injection of the selenite [2].
• Direct detection of potential selenium delivery proteins by using an Escherichia coli strain unable to incorporate selenium from selenite into proteins [3].
• Inhibition of NF-kappaB DNA binding and nitric oxide induction in human T cells and lung adenocarcinoma cells by selenite treatment [4].
• The toxicity of selenite generally increased as the culture density increased [5].

Psychiatry related information on SODIUM SELENITE

• The effects of sublethal doses of selenite, selenate, selenocystine (Se-Cys) and selenomethionine (Se-Met) as well as of tellurite on body temperature and feeding behavior were examined in male ICR mice [6].
• The effect of 0.1 and 0.2 mg/kg sodium selenite on the TBARS level and thiol group in sleep centers was significantly opposite to the wakefulness center [7].
• Administration of sodium selenite either before or after global cerebral ischaemia markedly reduced cerebral infarct size and attenuated impairment in short-term memory and motor coordination [8].
• An advantage of selenomethionine is lower lethal and behavioral toxicity (locomotor activity depression) compared to sodium selenite, when they are administered at equivalent doses of Se [9].

High impact information on SODIUM SELENITE

• Partial replacement of serum by selenite, transferrin, albumin and lecithin in haemopoietic cell cultures [10].
• A strain of Bacillus megaterium isolated from soil has been found to oxidize elemental selenium in laboratory cultures to selenite and a trace of selenate (< 1 percent of the selenite) [1].
• Selenite, another effective chemopreventive agent in this tumor model, also requires AdoMet for its metabolism [11].
• New approaches to cancer chemoprevention with difluoromethylornithine and selenite [11].
• These mouse mammary cell lines were derived from mid-pregnant primiparous BALB/c female mice and were routinely grown in Dulbecco's modified Eagle medium supplemented with 1% fetal bovine serum, insulin, transferrin, epidermal growth factor, and selenite [12].

Chemical compound and disease context of SODIUM SELENITE

• Antioxidants, including bovine liver catalase, bovine erythrocyte CuZn-SOD, sodium selenite and Trolox, a water soluble vitamin E analogue, as well as hypoxia, inhibited dexamethasone-induced apoptosis [13].
• These observations led us to investigate the abiotic (chemical) reduction of selenite by glutathione and to compare the features of this reaction with those of the reaction mediated by R. rubrum and E. coli [14].
• In contrast, extracellular formation of hydrogen selenide can fully explain the exacerbation of selenite toxicity by thiols [15].
• We have investigated whether selenite alone and in combination with doxorubicin induced apoptosis in variously differentiated mesothelioma cells [16].
• We have shown that selenite inhibits cell growth and induces apoptosis in androgen-dependent LAPC-4 prostate cancer cells [17].

Biological context of SODIUM SELENITE

• However, higher concentrations (10 microM) of selenite had no effect on oxidant-induced sister chromatid exchange formation, and 0.1 mM selenite increased the number of exchanges [18].
• Approximately 2 days after administration of the selenite the Tc decreased sharply to a minimum, and then at day 4 the Tc increased dramatically toward body temperature [2].
• In addition, 10 microM gold(I) or 10 microM selenite inhibited expression of an AP-1-dependent reporter gene, but not an AP-2-dependent reporter gene [19].
• Prior alkylation of the cysteine thiol groups in reduced rSeBP prevented selenite reduction and selenium binding under comparable conditions [20].
• After acute exposure to selenite, cells exhibited mitochondrial injury and cell death, mainly apoptosis [21].

Anatomical context of SODIUM SELENITE

• This hypothesis was indirectly supported by tissue selenium measurements showing that 0.5 or 0.25% of vitamin C in the diet completely negated in blood, liver, and mammary gland the accumulation of selenium induced by 3 ppm of selenite supplementation [22].
• We found that the addition of sodium selenite and sodium selenate inhibited the growth of human 3B6 and BL41 lymphocytes [23].
• After chronic exposure to selenite, cells showed growth inhibition caused by cell cycle arrest, increased numbers of mitochondria and levels of mitochondrial enzymes, and only minimal induction of apoptosis [21].
• Brief pre-exposure of HeLa cells to micromolar concentrations of selenite resulted in a dose-dependent decrease in the rate of their subsequent attachment to a solid matrix (tissue culture dish) [24].
• LNCaP cells treated with selenite also showed p53 translocation to mitochondria, cytochrome c release into the cytosol, and activation of caspase-9 [25].

Associations of SODIUM SELENITE with other chemical compounds

• Formation of a selenium-substituted rhodanese by reaction with selenite and glutathione: possible role of a protein perselenide in a selenium delivery system [26].
• Proportional inhibition of iNOS activity as measured by decreased NO products in the medium (NO2- and NO3-) resulted from selenite addition to cell suspensions [4].
• The relative effectiveness of either sodium selenite or selenomethionine in the inhibition of mammary carcinogenesis was studied in virgin female Sprague-Dawley rats [27].
• Two SE compounds were tested: selenodiglutathione (SDG), the primary metabolite of selenite and the most commonly used cancer-protective SE compound in animal models, and the synthetic SE compound, 1,4-phenylenebis(methylene)selenocyanate (p-XSC), one of the most potent chemopreventive pharmacological SE compounds [28].
• LNCaP cells also showed sequential increases in levels of phosphorylated p53 (serine 15), total p53, Bax, and p21(Waf1) proteins following selenite treatment [25].

Gene context of SODIUM SELENITE

• Selenophosphate synthetase genes from lung adenocarcinoma cells: Sps1 for recycling L-selenocysteine and Sps2 for selenite assimilation [29].
• We have investigated mechanisms by which selenium, in the form of sodium selenite, added to serum-free growth medium regulates TR activity in cancer cell lines [30].
• Furthermore, selenite directly inhibited JNK/SAPK activity in vitro but not the p38 activity [31].
• In contrast, selenite had little effect on the extracellular signal-regulated kinase pathway [31].
• Intriguingly, in this study we found a tight correlation between selenite resistance and expression of the high affinity orthophosphate carrier Pho84p [32].

Analytical, diagnostic and therapeutic context of SODIUM SELENITE

• The mechanism(s) that accounts for the heightened efficacy of combined DFMO and selenite chemoprevention will be discussed [11].
• The variation of the phase-separation temperature (Tc) was studied in lenses during formation of cataracts induced by a subcutaneous injection of sodium selenite [2].
• Immunoblotting analysis revealed that multiple proteins were up-regulated by chronic exposure to selenite [21].
• The effects of selenium exposure were studied in LNCaP human prostate cancer cells, and this same cell line adapted to selenium over 6 months to compare acute versus chronic effects of sodium selenite, the latter most closely resembling human clinical trials on the effects of selenium in cancer prevention and therapy [21].
• Subsequently, patients added 100 micrograms/day of selenious acid to their total parenteral nutrition solutions [33].

References