Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Selenium Oxides”

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 55 records · Page 3Linked to original sources
PubMed2005

Differential effects of selenite and selenate on human melanocytes, keratinocytes, and melanoma cells.

Among the substances that attracted the attention of oncologists in recent years are selenium-containing compounds, both inorganic and organic. Several epidemiological studies have shown an inverse correlation between selenium intake and cancer incidence. In the experiments reported here, we compared the effects of 2 inorganic selenium-containing salts that differed in the level of selenium oxidation, selenite IV and selenate VI. We tested the effects of these 2 compounds on cell survival and growth, cell cycle processing, cell morphology, cytoskeleton, and lipid peroxidation in 3 human skin cell types: normal keratinocytes, melanocytes, and human melanoma cell line HTB140. The different effects of selenite and selenate on the viability, growth, and morphology of normal cells and tumor cells are reported and provide a base for future research and treatment of some neoplastic diseases. The attention is paid to cell apoptosis induced by selenite and not by selenate, and the effects of tested substances on thioredoxin reductase system are postulated.

Adult↗
PubMed1983

Induction of retrovirus gene expression by selenium compounds.

Sodium selenite, sodium selenate, selenium oxide, selenophypoxanthine, selenopurine, selenocysteine, selenoethionine and selenomethionine were tested for their ability to induce endogenous retrovirus expression in cultured AKR mouse embryo fibroblasts. All except selenoethionine were highly toxic to the cells. Only selenomethionine however, had the ability to induce virus expression under the conditions used. The level of virus induction (plaque-forming-units/10(5) cells) was roughly proportional to dose over the range of concentrations from 0.25 mM to 5.0 mM. Induction was best observed when a treatment duration of 48 h was used and required the treatment of actively dividing cells. The induction and the cytotoxic effects of selenomethionine could be abrogated by simultaneous treatment with methionine. A ratio of methionine to selenomethionine of 1:10 inhibited induction by approx. 60% while equivalent amounts of methionine inhibited selenomethionine-mediated induction by greater than 96%, indicating that methionine was more efficiently recognized by the cells than was selenomethionine. A possible mechanism for selenomethionine induction involving the production of undermethylated DNA is presented.

Animals↗
PubMed1989

Radioactive-electrophoretic assay of adenosine 5'-triphosphate sulfurylase activity in crude extracts with sulfate or selenate as a substrate.

An assay method for ATP sulfurylase is presented which employs Na2(35)SO4 as a substrate and measures the production of labeled adenosine 5'-phosphosulfate and 3'-phosphoadenosine 5'-phosphosulfate by low-voltage, hanging paper strip electrophoresis. The method is applicable to crude bacterial or mammalian extracts and accurately measures picomole amounts of product(s). Na2(75SeO4 can also be employed as a substrate, if the unstable radioactive product, adenosine 5'-phosphoselenate, is converted to elemental 75Se degrees by inclusion of reduced glutathione in the reaction mixture. The same paper strip electrophoretic technique can then be used to separate 75Se degrees from the radiolabeled substrate. The method also has utility for measuring any direct reduction by crude microbial extracts of radioactive selenate to selenite, independent of ATP sulfurylase.

Adenosine Phosphosulfate↗
PubMed1989

Design, synthesis and 64Cu labeling of fatty acid analogs containing dithiosemicarbazone chelate.

For the development of 62Cu labeled fatty acid analogs, two fatty acid analogs, containing dithiosemicarbazone (DTS) molecule as the 62Cu coordinating site, were designed and synthesized: a fatty acid analog containing DTS molecule at the omega-position, (a) the 12,13-dioxotetradecanoic acid di(N-methyl-thiosemicarbazone) (FA-DTS), and an omega-phenyl fatty acid analog containing DTS molecule at the para-position, (b) the p-carboxyundecylphenylglyoxal-di (N-methylthiosemicarbazone] (PFA-DTS). FA-DTS was synthesized by the reaction of ethyl diethoxyacetate with ethyl 11-bromonundecanate by successive decarboxylation and hydrolysis and final condensation with N-methylthiosemicarbazide. PFA-DTS was synthesized by the Friedel-Craft acylation of ethyl 11-phenylundecanate, selenium oxidation of the acetophenone derivative, followed by the condensation with N-methylthiosemicarbazide. Radiolabeling of FA-DTS and PFA-DTS with [64Cu]copper acetate was simple, rapid and quantitative. When injected into mice, both compounds were distributed and retained in the myocardium. These results offer a good basis for further development of 62Cu labeled fatty acid analogs.

Animals↗
PubMed1995

Synthesis of saframycins. X. Transformation of (-)-saframycin A to (-)-saframycin Mx type compound with the structure proposed for saframycin E.

Treatment of (-)-saframycin A (1a) with selenium oxide in acetic acid afforded (-)-saframycin G (1g), and a catalytic reduction and regioselective oxidation sequence afforded the saframycin Mx type compound (3). We applied this methodology to the transformation of (+/-)-5-hydroxysaframycin B (11) to the hydroquinone (1e). Acetylation of 1e with acetic anhydride in pyridine gave the triacetate (13), which is identical with the triacetyl derivative of natural saframycin E.

Anti-Bacterial Agents↗
PubMed1992

Simultaneous induction of interferon gamma and tumor necrosis factor alpha by different seleno-organic compounds in human peripheral blood leukocytes.

Ebselen is known as anti-inflammatory and anti-oxidant selenium containing drug. We have synthetized 13 seleno-organic compounds, analogs of ebselen. Seven of them were found to be inducers of interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) in human peripheral blood leukocytes (PBL) cultures. The most active cytokine inducers were: 2-phenyl-1,2-benzisoselenazol-3(2H)-one (1, ebselen), bis [2-(N-phenylcarbamoyl)]phenyl diselenide (7) and bis (2-[N-(2-pyridyl)carbamoyl])phenyl diselenide (8). The amounts of IFN and TNF produced by PBL cultures in response to the seleno-organic compounds were found to be similar to that induced by phytohemagglutinin (PHA). The activities of the seleno-organic compounds were dose-dependent and related to the chemical structure of the drugs suggesting involvement of the specific cytokine-inducer receptor. The simultaneous inductions of IFN-gamma and TNF-alpha were highly correlated, but independent on each other.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

[Blood platelets, lipid peroxidation and antioxidants].

The paper reviews published data on the products of platelet lipid peroxidation, their role in blood coagulation as other physiological and pathological processes. The authors discuss the significance of anti-oxidants (selenium, glutathione peroxidase, reduced glutathione and vitamin E) in removing excessive hydroperoxides and thus in the control of platelet functional activity. Changes in platelet arachidonic acid metabolites and in antioxidants were found in a number of pathological conditions such as diabetes mellitus and cardiovascular diseases.

Animals↗
PubMed1989

[Synthetic studies of substituted quinazolinone].

We re-examined 2-methyl-3-(2-chlorophenyl)-6-ethoxycarbonyl-5,7-dimethyl-4 (3H)-quinazolinone to be hydroxymethylated by means of selenium oxide oxidation, followed by Ca (BH4)2 reduction. Chlorination reaction of 2-hydroxymethyl quinazolinone proceeded effectively by use of PCl5 in anhyd. benzene at room temperature. Thus, we prepared new compounds in respect of substituted quinazolinone.

Quinazolines↗
PubMed1983

Comparative activation response of splenocytes oxidized by periodic acid and selenium dioxide.

Murine splenocytes were activated by selenium dioxide (SeO2) oxidation of cell membranes, as evidenced by increased tritiated thymidine (3H-TdR) incorporation. In contrast to splenocyte activation by periodic acid (H5IO6), the SeO2-induced response was not inhibited by neuraminidase degradation of cell membranes prior to oxidation, nor by the prior hydroxylamine (NH2OH) addition reaction. However, reduction by borohydride (NaBH4), as a preliminary step to the oxidation by SeO2 and H5IO6, inhibited the subsequent cell activation. Sequential oxidation by H5IO6 and SeO2 increased the cell stimulation index versus the response elicited after one step oxidation by SeO2 or H5IO6. The reverse order of the sequential oxidation depressed the stimulation index relative to oxidation solely by H5IO6, but not by SeO2. It is concluded that the activation of splenocytes by SeO2 is triggered primarily by the conversion of cell membrane carbonyls into corresponding dicarbonyls.

Animals↗
PubMed1999

Oxidative stress during selenium deficiency in seedlings of Trigonella foenum-graecum and mitigation by mimosine Part II. Glutathione metabolism.

Adaptive alterations in glutathione (GSH) metabolism were studied during oxidative stress induced by selenium (Se) deficiency in germinating seedlings of Trigonella foenum-graecum grown for 72 h and the response to supplementation individually of Se or mimosine was explored. Growth enhancement with improved mitochondrial efficiency was elicited by supplementation of Se at 0.5-0.75 ppm or mimosine at 0.1-0.2 mM. Total thiol and protein levels of mitochondrial and soluble fractions, in general, did not vary significantly with supplementation of either Se or mimosine except that the mitochondrial protein levels in mimosine groups (0.1-0.2 mM) decreased by 20-30%. Mitochondrial glutathione peroxidase (GSH-Px) increased by twofold in activity toward H2O2, cumene hydroperoxide (CHP), and t-butyl hydroperoxide (tBHP) in Se groups, and by 50-60% increase toward H2O2 and CHP but by a twofold enhancement in enzyme activity with tBHP in mimosine groups. Soluble GSH-Px activity increased by 30-40% only in mimosine groups and remained unaltered in Se groups. Glutathione S-transferase activity (GST) in the soluble fraction of both Se and mimosine groups increased dramatically by fivefold to sixfold. Distinct differences were noted in the response of the stressed seedlings toward exposure to Se or mimosine and included a decline in glutathione reductase (GR) activity by 50-60% in both mitochondria and soluble fractions of Se groups and an increase in GR activity of the mitochondria by twofold and of the soluble enzyme activity by 30% in the mimosine groups. Mimosine exposure resulted in a dose-dependent decrease in the gamma-glutamyl transpeptidase levels, but, in contrast, a significant enhancement by 50% was noted in the Se group at 0.75 ppm. The results including the differential response of GR activity to Se or mimosine supplementation are reflective of an effective reductive environment in Se groups and increased turnover of GSH in the presence of mimosine.

Glutathione↗
PubMed2005

Melatonin-selenium nanoparticles inhibit oxidative stress and protect against hepatic injury induced by Bacillus Calmette-Guérin/lipopolysaccharide in mice.

Melatonin-selenium nanoparticles (MT-Se), a novel complex, were synthesized by preparing selenium nanoparticles in melatonin medium. The present investigation was designed to determine the protective effects of MT-Se against Bacillus Calmette-Guérin (BCG)/lipopolysaccharide (LPS)-induced hepatic injury in mice. In BCG/LPS-induced hepatic injury model, MT-Se administered (i.g.) at doses of 5, 10, or 20 mg/kg to BCG/LPS-treated mice for 10 days, significantly reduced the increase in plasma aminotransferase, reduced the severe extent of hepatic cell damage and the immigration of inflammatory cells. The MT-Se particles also attenuated the increase in the content of thiobarbituric acid-reactive substances and enhanced the decrease in reduced activities of superoxide dismutase and glutathione peroxidase (GPx). However, treatment with MT-Se suppressed the increase in nitric oxide levels both in plasma and liver tissue. Furthermore, supplementation with MT-Se at the dose of 10 mg/kg (composed of 9.9 mg/kg melatonin and 0.1 mg/kg selenium) had great capability to protect against hepatocellular damage than a similar dose of melatonin (10 mg/kg) or selenium (0.1 mg/kg) alone. This effect may relate to its higher antioxidant efficacy in decreasing lipid peroxidation and increasing GPx activity. These results suggest that the mode of MT-Se hepatic protective action is, at least in part, related to its antioxidant properties.

Animals↗
PubMed2002

The effects of vitamin E and selenium intake on oxidative stress and plasma lipids in hamsters fed fish oil.

The aim of the present work was to test the effects of large-dose supplementation of vitamin E (Vit E) and selenium (Se), either singly or in combination, on fish oil (FO)-induced tissue lipid peroxidation and hyperlipidemia. The supplementation of Se has been shown to lower blood cholesterol and increase tissue concentrations of the antioxidant glutathione (GSH); however, the effects of Se supplementation, either alone or in combination with supplemental Vit E, on FO-induced oxidative stress and hyperlipidemia have not been studied. Male Syrian hamsters received FO-based diets that contained 14.3 wt% fat and 0.46 wt% cholesterol supplemented with Vit E (129 IU D-alpha-tocopheryl acetate/kg diet) and/or Se (3.4 ppm as sodium selenate) or that contained basal requirements of both nutrients. The cardiac tissue of hamsters fed supplemental Se showed increased concentrations of lipid hydroperoxides (LPO) but decreased oxidized glutathione (GSSG) concentrations. The higher concentrations of LPO in the hearts of Se-supplemented hamsters were not lowered with concurrent Vit E supplementation. In the liver, Se supplementation was associated with higher Se-dependent glutathione peroxidase activity and an increase in the GSH/GSSG ratio, whereas a lower hepatic non-Se-dependent glutathione peroxidase activity was seen with Vit E supplementation. Supplemental intake of Se was associated with lower plasma concentrations of total cholesterol and low density lipoprotein cholesterol plus very low density lipoprotein cholesterol. In view of the pro-oxidative effects of Se supplementation on cardiac tissue, a cautionary approach needs to be taken regarding the plasma lipid-lowering properties of supplemental Se.

Animals↗
PubMed2004

The impact of cardiopulmonary bypass on selenium status, thyroid function, and oxidative defense in children.

Selenium has important functions for oxidative defense and thyroid hormone metabolism. Selenium-dependent enzymes include 5'-iodothyronine deiodinase and glutathione peroxidase (GPX). The objective of this study was to investigate the relationship between plasma selenium, GPX activity, and thyroid hormone status in pediatric cardiac surgical patients. Plasma concentrations of selenium, free triiodothyronine (fT3), free thyroxin (fT4), and c-reactive protein as well as plasma activity of GPX were prospectively evaluated at anesthetic induction and 48 hours postoperatively in 59 children requiring cardiopulmonary bypass (CPB). GPX was measured at additional time points at 6, 12, and 24 hours postoperatively. There was a significant reduction in the plasma selenium concentration after cardiopulmonary bypass with obtained median measurements of 0.61 micromol/L (induction) and 0.51 micromol/L (48 hours postoperatively). The fT3/fT4 ratio decreased significantly from 0.28 at anesthetic induction to 0.22 at 48 hours postoperatively. There were no significant changes of GPX activity. 48 hours fT3 concentration, fT3/fT4 ratio, and selenium concentration were significantly negatively correlated with the time spent in intensive care. The concentration of plasma selenium in children undergoing cardiopulmonary bypass significantly decreases, resulting in diminished deiodinase activity, and a subsequent reduction in the conversion of T4 to T3.

Adolescent↗
PubMed2003

Intravenous n-acetylcysteine, ascorbic acid and selenium-based anti-oxidant therapy in severe acute pancreatitis.

BACKGROUND: To observe outcome in a cohort of patients with severe acute pancreatitis receiving multiple anti-oxidant therapy. METHODS: An observational study was carried out in 46 consecutive patients with acute pancreatitis fulfilling current Atlanta consensus criteria for severe disease. All patients received multiple anti-oxidant therapy based on intravenous selenium, N-acetylcysteine and ascorbic acid plus beta-carotene and alpha-tocopherol delivered via nasogastric tube. Principal outcomes were the effect of anti-oxidant supplementation on anti-oxidant levels, morbidity and mortality in patients on anti-oxidant therapy, case-control analysis of observed survival compared to predicted survival derived from logistic organ dysfunction score (LODS), logistic regression analysis of factors influencing outcome and side effect profile of anti-oxidant therapy. RESULTS: Paired baseline and post-supplementation data were available for 25 patients and revealed that anti-oxidant supplementation restored vitamin C (P = 0.003) and selenium (P = 0.028) toward normal. In univariate survival analysis, patient survival to discharge was best predicted by admission APACHE-II score with relative risk of death increasing 12.6% for each unit increase (95% CI 6.0% to 19.6%). The mean LODS calculated on admission to hospital was 3.7 (standard error of the mean 4.1) giving a predicted mortality for the cohort of 21%. The observed in-hospital mortality was 43%. CONCLUSIONS: Case-control analyses do not appear to demonstrate any benefit from the multiple anti-oxidant combination of selenium, N-acetylcysteine and ascorbic acid in severe acute pancreatitis.

Acetylcysteine↗
PubMed2005

Correlation between ketone body level in selenium-deficient rats and oxidative damages.

The age dependence of ketone body levels (KBLs) and oxidative damages in selenium-deficient (SeD) and normal rats were compared. The feeding SeD diets gave ketogenesis and higher KBLs especially in younger rats. However, KBLs in SeD rats seemed to decrease with their age. Feeding 0.1 mg/kg Se in water with SeD diet did not affect the KBLs in young (8 week old) rats, whereas the addition of Se reduced the KBLs in older (20 week old) rats. Blood KBLs showed some correlations with tissue damage. TBARSs showed no correlations with the tissue damages and KBLs when the values were compared between the same age, while better correlation was obtained between urinary KBLs of 6-20 week old normal rats and the liver TBARSs of 4-16 week old normal rats. The oxidative injury might induce liver damage with some delay. SeD rat kidney TBARS levels normalized by protein had some correlations with BUN and blood KBL. Kidney may be sensitive to the oxidative stresses and/or injuries. Tissue damages of SeD rats decreased with age. In contrast, oxidative injuries might be gradually accumulated in normal rat tissue. Oxidative stress can be visible by gradual accumulation of small damages during the aging, while large stress in young rats can be buffered and masked. The aging based accumulation of oxidative injuries might also be correlated with KBLs, while it might not give notable tissue damages.

Animals↗