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 379 records · Page 21Linked to original sources
PubMedDate not supplied

Antioxidant micronutrients in children with thalassaemia in Egypt.

Repeated blood transfusions in patients with thalassaemia subject them to peroxidative tissue injury by secondary iron overload. To study the relationship between iron overload and antioxidant micronutrient status among children with thalassaemia, we measured serum levels of vitamins A and E, zinc, selenium, and copper in 64 children with beta-thalassaemia major and 63 age- and sex-matched controls. All of these elements were significantly lower in the thalassaemic children compared with controls. There was a highly significant inverse correlation between serum ferritin and serum retinol levels, and significant inverse correlations between serum iron and retinol and between serum iron and selenium. Serum ferritin showed a significant positive correlation with duration of chelation and transfusion treatments. Ways are needed to counteract this oxidative damage and its deleterious effect on the prognosis of thalassaemia.

Adolescent↗
PubMed1997

A T-cell model for the biological role of selenium-dependent glutathione peroxidase.

The cytosolic form of selenium-dependent glutathione peroxidase detoxifies both hydrogen and lipid peroxides and therefore represents a major component of the cellular anti-oxidant defenses. In order to study the biological role of this enzyme, we generated an expression construct in a retroviral vector, which when introduced into immortalized human T-cells, resulted in significant increases in the activity of this important enzyme. This effect is stable over extended maintenance in culture. The anti-oxidant defenses in these same cells are also shown to be attenuated by chemically reducing cellular glutathione levels. Collectively, the ability to both increase and decrease the anti-oxidant defenses in human T cells results in a useful model system for the study of oxidative stress and signaling in this cell type.

Cell Line↗
PubMed2001

Selenium spares ascorbate and alpha-tocopherol in cultured liver cell lines under oxidant stress.

The selenoenzyme thioredoxin reductase (TR) can recycle ascorbic acid, which in turn can recycle alpha-tocopherol. Therefore, we evaluated the role of selenium in ascorbic acid recycling and in protection against oxidant-induced loss of alpha-tocopherol in cultured liver cells. Treatment of HepG2 or H4IIE cultured liver cells for 48 h with sodium selenite (0-116 nmol/l) tripled the activity of the selenoenzyme TR, measured as aurothioglucose-sensitive dehydroascorbic acid (DHA) reduction. However, selenium did not increase the ability of H4IIE cells to take up and reduce 2 mM DHA, despite a 25% increase in ascorbate-dependent ferricyanide reduction (which reflects cellular ascorbate recycling). Nonetheless, selenium supplements both spared ascorbate in overnight cultures of H4IIE cells, and prevented loss of cellular alpha-tocopherol in response to an oxidant stress induced by either ferricyanide or diazobenzene sulfonate. Whereas TR contributes little to ascorbate recycling in H4IIE cells, selenium spares ascorbate in culture and alpha-tocopherol in response to an oxidant stress.

Animals↗
PubMed2006

Effect of selenium on Cisplatin-induced nephrotoxicity in rats.

Cisplatin (CP), a commonly used antineoplastic drug, is nephrotoxic. CP-induced nephrotoxicity involves oxidative pathways. A deficiency of selenium (Se) reduces glutathione peroxidase (GPx) activity resulting in oxidative stress. We investigated how Se deficiency or oral Se administration influences CP-induced nephrotoxicity. Thirty male Wistar rats were fed a Se-deficient or control diet for 4 weeks. Then they were given intraperitoneal (i.p.) CP alone, i.p. saline alone, or Se by gavage 24 and 1 h prior to i.p. CP. Blood and urine samples were collected and the kidneys were removed 5 days after CP treatment. Urinalysis, renal function, GPx activity, and expression of cellular GPx mRNA were measured. Histology was evaluated by light microscopy with immunohistochemistry for 4-hydroxy-2-nonenal (HNE), vimentin, and heme oxygenase (HO)-1. CP induced renal tubular damage with increased expression of vimentin, HO-1 and HNE staining, which represents lipid peroxidation. Se deficiency exacerbated CP-induced nephrotoxicity as shown by deterioration of the above parameters and depressed GPx activity and expression of GPx mRNA. Se treatment ameliorated CP-induced nephrotoxicity, but did not significantly improve renal function. These findings suggest that Se deficiency increases oxidative stress and enhances CP-induced nephrotoxicity, whereas oral Se treatment partially protects against the nephrotoxicity in rats.

Administration, Oral↗
PubMed2006

The role of selenium in thyroid autoimmunity and cancer.

The essential micronutrient selenium (Se) occurs in the form of the amino acid selenocysteine in selenoproteins which exert various effects, while maintaining the cell reduction-oxidation balance. The discovery that all three deiodinases that convert thyroxine (T4) into triiodothyronine (T3) contain selenocysteine illustrates how the production of the active thyroid hormone is dependent on Se status. The selenoenzyme families of glutathione peroxidases (GPx) and thioredoxin reductases (TRx) possess powerful antioxidant properties and form a complex defense system that protects thyrocytes from oxidative damage. Se supplementation in patients with autoimmune thyroiditis seems to modify the immune response, probably by enhancing plasma GPx activity and decreasing excess levels of hydrogen peroxide. However, the enhancement of immunocompetence may also be the result of the synergistic action of various selenoproteins and not exclusively of GPx. There is evidence supporting considerable oxidative stress in Graves' disease where Se supplementation, because of its free radical scavenging properties, may increase the enzymatic antioxidant activity. TRx has been found significantly elevated in GD revealing its involvement in the pathogenesis of this condition and representing a potential future target for therapeutical intervention. Low Se serum levels have also been associated with increased risk of thyroid cancer and may play a role in carcinogenesis. It is noteworthy, that the Food and Drug Administration has recently determined that there is sufficient evidence to warrant a qualified health claim for Se and cancer. Furthermore, the recent discovery that defects in the SECIS-binding protein 2 (SBP2), which is an indispensable protein for the incorporation of Se into the selenoproteins, result in thyroid dysfunction, together with the recognition of the many roles of selenoprotein P in Se distribution and storage in the human body, reveal not only the indispensability of Se and the selenoproteins as essential factors in thyroid metabolism and pathogenesis, but open up new prospects for enhanced treatment.

Animals↗
PubMed1990

[Study of oxidative damage on mitochondrial membrane of myocardium deficient in selenium].

Keshan disease (KD) is an endemic cardiomyopathy with membrane damage of the myocardial mitochondria. This paper reports the results of feeding guinea pigs with a forage obtained from KD endemic area. The selenium (Se) content and glutathione peroxidase activity in blood, tissues, mitochondria, microsome and supernatant of myocardium and liver cells of the experimental group were decreased. Additionally, the activity of glutathione-S-transferase was also decreased to some extent, instead of being increased in normal cases, and the content of lipid peroxide and hydroperoxide was increased. At the same time, cardiolipin in mitochondria, and the activity of cytochrome C oxidase (CCO, an enzyme binding with mitochondrial membrane) were also reduced accompanied with oxidative damage and disorder of function of the membrane. Anyhow, when exogenous cardiolipin was added in the purified endemic CCO solution, it was capable of restoring CCO activity significantly. The significance of Se deficiency and unbalanced diet in pathogenesis of Keshan disease is discussed.

Animals↗
PubMed2006

Comparative toxicosis of sodium selenite and selenomethionine in lambs.

Excess consumption of selenium (Se) accumulator plants can result in selenium intoxication. The objective of the study reported here was to compare the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (sodium selenite). Lambs were orally administered a single dose of selenium as either sodium selenite or selenomethionine and were monitored for 7 days, after which they were euthanized and necropsied. Twelve randomly assigned treatment groups consisted of animals given 0, 1, 2, 3, or 4 mg of Se/kg of body weight as sodium selenite, or 0, 1, 2, 3, 4, 6, or 8 mg of Se/kg as selenomethionine. Sodium selenite at dosages of 2, 3, and 4 mg/kg, as well as selenomethionine at dosages of 4, 6, and 8 mg/kg resulted in tachypnea and/or respiratory distress following minimal exercise. Severity and time to recovery varied, and were dose dependent. Major histopathologic findings in animals of the high-dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Analysis of liver, kidney cortex, heart, blood, and serum revealed linear, dose-dependent increases in selenium concentration. However, tissue selenium concentration in selenomethionine-treated lambs were significantly greater than that in lambs treated with equivalent doses of sodium selenite. To estimate the oxidative effects of these selenium compounds in vivo, liver vitamin E concentration also was measured. Sodium selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Results of this study indicate that the chemical form of the ingested Se must be known to adequately interpret tissue, blood, and serum Se concentrations.

Animals↗
PubMed1986

Lipid peroxides in blood plasma and enzymatic antioxidative defence of erythrocytes in Down's syndrome.

The level of lipid peroxides was significantly increased in the blood of patients with Down's syndrome. In erythrocytes increased activities of superoxide dismutase and glutathione peroxidase were confirmed while catalase activity was similar to that of healthy controls. The concentration of selenium in erythrocytes of Down's syndrome patients was reduced, in spite of increased glutathione peroxidase activity. These results confirm the hypothesis of an altered oxidative metabolism in Down's syndrome.

Catalase↗
PubMed2006

Accumulation of mercury, selenium and their binding proteins in porcine kidney and liver from mercury-exposed areas with the investigation of their redox responses.

The subcellular localization of Se and Hg and their cytosolic binding proteins, including cellular oxidative status, in porcine liver and kidney have been studied by using samples from a chronic Hg-contaminated area and a non-Hg-contaminated area. Coaccumulation and redistribution of Se and Hg in subcellular fractions due to mercury exposure were found. The Hg and Se concentrations in tissues from Hg-exposed porcine were 80 fold and 5-20 fold higher than controls, respectively. Interestingly, the retention of both Se and Hg increased 10% in mitochondria, while decreased 10% in cytosol of Hg-exposed pig liver. Mercury was mainly in the form of MTs in the cytosol of the non-Hg-exposed porcine kidney. MT binds Hg in the cytosol with limited capacity, and the rest Hg was redistributed to the high molecular weight (MW) proteins (80-100 kDa) in the Hg-exposed group. The coaccumulation of Hg and Se was also found in high MW proteins, where their molar ratio tended to be 1:1. Moreover, the Se-containing polypeptides (3-6 kDa) increased significantly both in hepatic and renal cytosol of the Hg-exposed pigs. Se-dependent GSH-Px and SOD activity were increased to cope with Hg-induced oxidative stress. In previous studies, the roles of Se and MTs were generally taken into account separately; we discussed their combining roles in the case of high Hg exposure. The present results were beneficial to understand the existing states of Hg in vivo and evaluate the interaction of toxic and essential elements.

Animals↗
PubMed2004

Selenomethionine stimulates MAPK (ERK) phosphorylation, protein oxidation, and DNA synthesis in gastric cancer cells.

Selenium is an essential trace element and is required for the synthesis of cellular enzymes that protect against oxidative stress. Epidemiological findings indicate that low selenium intake is associated with increased cancer risk, and, although the majority of studies show that exposure of transformed cells to selenium results in apoptotic cell death, there are reports indicating that cells exposure to low selenium concentrations promotes cellular proliferation. Gastric adenocarcinoma SNU-1 cells responded to selenomethionine with a biphasic proliferative curve: enhanced incorporation of 3H-thymidine into DNA within a very narrow range of selenomethionine concentrations followed by decreased 3H-thymidine uptake at higher levels. Concentrations of selenomethionine that stimulate cellular proliferation also induce cellular oxidation and phosphorylation of MAPK (ERK), a component of cell signaling cascades. MAPK (ERK) phosphorylation is synonymous with MAPK activation and enhanced cell growth. Our findings support previous observations of enhanced proliferation in response to low levels of selenium and suggest that, at certain concentrations, selenomethionine induces mild oxidative stress that, in turn, stimulates DNA synthesis.

Adenocarcinoma↗
PubMed1996

Roles of multiple oxidized LDL lipids in cellular injury: dominance of 7 beta-hydroperoxycholesterol.

The relative toxicities of several lipid oxidation products formed on oxidized LDL, their presence on oxidized LDL, and potential mechanisms of cell injury compared to oxidized LDL were examined. Toxicities to fibroblasts, with lipoprotein-deficient serum supplementation, were: 7 beta-hydroperoxycholesterol > 7 beta-hydroxycholesterol = 4-hydroxynonenal > 7-ketocholesterol > 5 alpha, 6 alpha-epoxycholesterol. Lysophosphatidylcholine was only significantly cytotoxic in the absence of lipoprotein-deficient serum. Without serum, relative toxicities were: 7 beta-hydroperoxycholesterol > lysophosphatidylcholine > 4-hydroxynonenal > 7 beta-hydroxycholesterol. Similar relative potencies were observed in smooth muscle and endothelial cell cultures. 7 beta-Hydroperoxycholesterol accumulated on oxidized LDL to greater amounts than other oxysterols and 4-hydroxynonenal, but less than lysophosphatidylcholine. Cell injury by 7 beta-hydroperoxycholesterol and oxidized LDL was inhibitable by antioxidants but not by exogenous cholesterol or cycloheximide. In contrast, a) toxicities by 7 beta-hydroxycholesterol, 7-ketocholesterol, 5 alpha, 6 alpha-epoxycholesterol, and 4-hydroxynonenal were not inhibited by antioxidants; b) 7 beta-hydroxycholesterol and lysophosphatidylcholine toxicities were inhibited by exogenous cholesterol; and c) 7 beta-hydroxycholesterol toxicity was inhibited by cycloheximide. Injury by lysophosphatidylcholine was reduced by vitamin E and not affected by altering the cellular exposure to selenium; reduced selenium enhanced toxicity by oxidized LDL and 7 beta-hydroperoxycholesterol. The high relative toxicity of 7 beta-hydroperoxycholesterol, the level of its accumulation on oxidized LDL, and its mechanism of action similar to oxidized LDL suggest that it is the compound predominantly responsible for oxidized LDL induced cytotoxicity.

Cells, Cultured↗
PubMed2000

Effects of selenium dioxide on blood and femoral bone marrow of rats.

This study was undertaken to investigate the effects of selenium dioxide (SeO2) on rat blood and femoral bone-marrow oxidant mechanisms. Treatment with SeO2, 67 microg Se/kg i.p. daily for 14 d, significantly decreased lipid peroxidation and the concentrations of Fe in serum and bone marrow. The concentrations of Se in serum and bone-marrow cells were significantly increased after SeO2 treatment. The activities of glutathione peroxidase (GPx) in blood and bone-marrow cells were markedly increased. The levels of oxyhemoglobin in blood were significantly increased, while the concentrations of methemoglobin were decreased after SeO2 administration. The fragility of erythrocytes membranes was significantly decreased in SeO2-treated rats compared to controls. Data suggest that treatment with a low dose of SeO2 may provide antioxidant nutrients to blood and bone marrow.

Animals↗
PubMed1991

Changes in ornithine decarboxylase activity and polyamine levels in response to eight different forms of selenium.

The biological activity of selenium is known to depend on its chemical form. In this study, eight forms of selenium that differed in oxidation state or degree of methylation were studied for their acute effects on the activities of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (AdoMet DC) and on the concentrations of the polyamines putrescine, spermidine, and spermine in the liver. The polyamine pathway was studied because it is involved in the control of cell growth and in the cell's response to trophic, carcinogenic, and toxic stimuli, activities that selenium has been reported to affect. Female Sprague Dawley rats were administered 12 mumol Se/kg body weight via intraperitoneal injection and were sacrificed six hours later. Injection of sodium selenate, sodium selenite, selenomethionine, Se-methylselenocysteine, selenobetaine, and selenobetaine methyl ester resulted in significant increases in liver selenium, whereas injection of dimethylselenoxide and trimethylselenonium chloride did not. ODC activity and AdoMet DC activity were induced by those selenium compounds that also increased liver selenium content, but the magnitude of enzyme induction by those compounds was not correlated with the hepatic concentration of total selenium determined fluorometrically. Furthermore, the induction of ODC activity by the various forms of selenium did not result in concomitant increases in putrescine, spermidine, and spermine except in the case of selenite. Given that alterations in the metabolism of selenium are induced when the level of tissue selenium is elevated and that the relative abundance of various selenometabolites can be affected by the point of entry of selenium into intermediary metabolism, these data suggest that the changes that were observed in enzyme activities and polyamine levels are likely to be associated with the accumulation of a specific metabolite of selenium. The relevance of these findings to elucidation of the biological activities attributable to various forms of selenium is under investigation.

Adenosylmethionine Decarboxylase↗