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PubMed2001

Erythrocyte, plasma, and serum antioxidant activities in untreated toxic multinodular goiter patients.

Erythrocyte, plasma, and serum antioxidant activities were studied in patients with newly diagnosed and untreated toxic multinodular hyperthyroid goiter and compared to healthy control subjects. Erythrocyte antioxidant enzyme activities, glutathione, malondialdehyde, and ceruloplasmin levels were significantly increased, whereas serum vitamin E, plasma vitamin C, and selenium levels were decreased in hyperthyroid patients compared to control subjects. The findings show that untreated toxic multinodular goiter causes profound alterations in components of the antioxidant system in erythrocytes indicative of increased oxidative stress. Taken together, these data suggest that hyperthyroid patients may benefit from dietary supplements of antioxidants.

Adult↗
PubMed2001

Formation of a selenium-substituted rhodanese by reaction with selenite and glutathione: possible role of a protein perselenide in a selenium delivery system.

Selenophosphate is the active selenium-donor compound required by bacteria and mammals for the specific synthesis of Secys-tRNA, the precursor of selenocysteine in selenoenzymes. Although free selenide can be used in vitro for the synthesis of selenophosphate, the actual physiological selenium substrate has not been identified. Rhodanese (EC ) normally occurs as a persulfide of a critical cysteine residue and is believed to function as a sulfur-delivery protein. Also, it has been demonstrated that a selenium-substituted rhodanese (E-Se form) can exist in vitro. In this study, we have prepared and characterized an E-Se rhodanese. Persulfide-free bovine-liver rhodanese (E form) did not react with SeO(3)(2-) directly, but in the presence of reduced glutathione (GSH) and SeO(3)(2-) E-Se rhodanese was generated. These results indicate that the intermediates produced from the reaction of GSH with SeO(3)(2-) are required for the formation of a selenium-substituted rhodanese. E-Se rhodanese was stable in the presence of excess GSH at neutral pH at 37 degrees C. E-Se rhodanese could effectively replace the high concentrations of selenide normally used in the selenophosphate synthetase in vitro assay in which the selenium-dependent hydrolysis of ATP is measured. These results show that a selenium-bound rhodanese could be used as the selenium donor in the in vitro selenophosphate synthetase assay.

Animals↗
PubMed2006

Effect of pH on one-electron oxidation chemistry of organoselenium compounds in aqueous solutions.

Pulse radiolysis coupled with absorption detection has been employed to study one-electron oxidation of selenomethionine (SeM), selenocystine (SeCys), methyl selenocysteine (MeSeCys), and selenourea (SeU) in aqueous solutions. Hydroxyl radicals (*OH) in the pH range from 1 to 7 and specific one-electron oxidants Cl2*- (pH 1) and Br2*- (pH 7) have been used to carry out the oxidation reactions. The bimolecular rate constants for these reactions were reported to be in the range of 2 x 10(9) to 10 x 10(9) M(-1) s(-1). Reactions of oxidizing radicals with all these compounds produced selenium-centered radical cations. The structure and stability of the radical cation were found to depend mainly on the substituent and pH. SeM, at pH 7, produced a monomer radical cation (lambdamax approximately 380 nm), while at pH 1, a dimer radical cation was formed by the interaction between oxidized and parent SeM (lambdamax approximately 480 nm). Similarly, SeCys, at pH 7, on one-electron oxidation, produced a monomer radical cation (lambdamax approximately 460 nm), while at pH 1, the reaction produced a transient species with (lambdamax approximately 560 nm), which is also a monomer radical cation. MeSeCys on one-electron oxidation in the pH range from 1 to 7 produced monomer radical cations (lambdamax approximately 350 nm), while at pH < 0, the reaction produced dimer radical cations (lambdamax approximately 460 nm). SeU at all the pH ranges produced dimer radical cations (lambdamax approximately 410 nm). The association constants of the dimer radical cations of SeM, MeSeCys, and SeU were determined by following absorption changes at lambdamax as a function of concentration. From these studies it is concluded that formation of monomer and dimer radical cations mainly depends on the substitution, pH, and the heteroatoms like N and O. The availability of a lone pair on an N or O atom at the beta or gamma position results in monomer radical cations having intramolecular stabilization. When such a lone pair is not available, the monomer radical cation is converted into a dimer radical cation which acquires intermolecular stabilization by the other selenium atom. The pH dependency confirms the role of protonation on stabilization. The oxidation chemistry of these selenium compounds is compared with that of their sulfur analogues.

Cystine↗
PubMed2006

Effect of selenium supplementation on biochemical markers and outcome in critically ill patients.

BACKGROUND & AIMS: This study aimed to assess the effect of high dose selenium (Se) supplementation on Se status in blood, oxidative stress, thyroid function and possible effects on requirement for renal replacement therapy (RRT) in severely septic patients admitted to the intensive care unit (ICU). METHODS: This prospective single-centre study was carried out in 40 septic ICU patients who were randomized to high dose Se (Se+ group, N=18 (474, 316, 158 microg/day), each for 3 consecutive days followed by a standard dose of 31.6 microg/day of Se given as sodium selenite whereas the control group (Se-, N=22) received only the standard dose of Se. Plasma Se, glutathione peroxidase (GSH-Px), F2 isoprostanes, thyroid function tests (total T4 and total T3), C-reactive protein (CRP) and red blood cell (RBC) GSH-Px were estimated on day 0, 3, 7, 14. RESULTS: In the Se+ group, plasma Se increased by day 3 and 7 (P<0.0001) and day 14 (P=0.02), plasma GSH-Px increased by day 3 and 7 (P=0.01) as compared to Se- group. There was a significant negative correlation between plasma Se and SOFA (sepsis related organ failure assessment) (r=-0.36, P=0.03) along with low plasma Se and high CRP at the time of admission. Requirement for renal replacement therapy was not significantly different between the groups. CONCLUSION: Although high dose Se supplementation increased plasma Se and GSH-Px activity, it did not reduce oxidative damage or the requirement for RRT. Se levels in blood are influenced by redistribution and severity of illness and therefore should be interpreted with caution.

Aged↗
PubMed2005

Aqueous extracts of selenium-fertilized broccoli increase selenoprotein activity and inhibit DNA single-strand breaks, but decrease the activity of quinone reductase in Hepa 1c1c7 cells.

Depending on growth conditions, broccoli may be enriched in the isothiocyanate sulforaphane and/or the mineral selenium (Se); both compounds may play an important role in the reduction of intracellular oxidative stress and chronic disease prevention. Sulforaphane up-regulates transcription of Phase II detoxification proteins (e.g. quinone reductase [QR]), whereas Se is needed for the production of thioredoxin reductase (TR) and glutathione peroxidase-1 (GPx1), both of which exhibit antioxidant activity. The objective of the present study was to determine whether the fertilization of broccoli with Se increases the antioxidant ability of broccoli. Hydrogen peroxide-induced DNA single-strand breaks (measured by single cell electrophoresis, Comet assay) and activity of antioxidant enzymes (GPx, TR and QR) were measured in mouse hepatoma cells (Hepa 1c1c7 cells) treated with purified sulforaphane, sodium selenite or extracts of selenized broccoli. When supplied separately as chemically pure substances, sodium selenite was more effective than sulforaphane for reduction of single-strand breaks. Se-fertilized broccoli extracts were the most effective for reduction of DNA single-strand breaks, and extracts that contained 0.71 microM Se and 0.08 microM sulforaphane inhibited 94% of DNA single-strand breaks. A significant positive association (r = 0.81, p = 0.009) between GPx1 activity and inhibition of DNA single-strand breaks as well as a 24h lag time between addition of Se, sulforaphane or broccoli extract and inhibition of single-strand breaks suggests that some of the antioxidant protection is mediated through selenoproteins. Conversely, fertilization of broccoli with Se decreased the ability of broccoli extract to induce QR activity. These results demonstrate that Se and sulforaphane, alone or as a component of broccoli, may help decrease oxidative stress. They further suggest that Se is the most important for decreasing oxidative stress, but maximizing the Se content of broccoli also may compromise its ability to induce Phase II detoxification proteins.

Antioxidants↗
PubMed2003

Kynurenine and neopterin in the aqueous humor of the anterior chamber of the eye and in serum of cataract patients.

Serum kynurenine, neopterin, selenium concentrations; neopterin concentrations in aqueous humour from anterior chamber of eye and selenium content in lenses were determined in 40 catarat patients with and in 51--without pseudoexfoliation (PES). Significantly increased kynurenine and neopterin levels in serum and neopterin concentration in aqueous humour were observed in mature cataract patients with PES compared to whose without. These patients also presented with the lowest content of selenium in serum and lens, compared with cataract patients without PES. Increased concentrations of neopterin in serum and aqueous humour of anterior chamber of eyes suggest an increased degree of oxidative stress in patients with PES. Thus, the results support the role of oxidative stress in the development of PES in cataract patients. The decreased content of selenium may elicit immune system activation via an increased oxidative stress as it is indicated by the increased formation of kynurenine and neopterin.

Aged↗
PubMed1994

Increase in oxidation resistance of atherogenic serum lipoproteins following antioxidant supplementation: a randomized double-blind placebo-controlled clinical trial.

OBJECTIVE: To test the effect of supplementation of diet with ascorbic acid, selenium, alpha-tocopherol and beta-carotene on the oxidation resistance of very low (VLDL) + low density lipoprotein (LDL). DESIGN: A randomized placebo-controlled double-masked clinical trial. SETTING: In healthy men aged 30-58 years smoking regularly 15-40 cigarettes/day. SUBJECTS: Forty subjects recruited from the general population, who all completed the study. INTERVENTION: 400 mg of slow release ascorbic acid, 100 micrograms of organic selenium, 200 mg of D-alpha-tocopheryl acetate and 30 mg of beta-carotene daily or placebo, 20 men in each group for 3 months. MAIN OUTCOME MEASURES: The oxidation resistance of VLDL + LDL measured by inducing oxidation with copper chloride and, separately, with a combination of haemin and H2O2. RESULTS: In plasma, alpha-tocopherol increased by 72%, beta-carotene by 209%, ascorbate by 45% and selenium by 20% in the supplemented men. The lag time to oxidation increased by 27% [95% confidence interval (CI) 18-35%, P < 0.001] after copper and by 29% (95% CI 12-46%, P = 0.002) after haemin plus H2O2 in the supplemented group as compared to the placebo group by t-tests. The respective net changes in the maximal oxidation velocity were a reduction of 10% (95% CI 1-21%, P = 0.037) after copper and a reduction of 15% (95% CI-1 to 30%, P = 0.070) after haemin and H2O2. CONCLUSIONS: These findings provide further confirmation for the notion that the supplementation of diet with antioxidative vitamins and selenium increases the oxidation resistance of atherogenic lipoproteins in human plasma.

Adult↗
PubMedDate not supplied

Induction of lipid peroxidation and alteration of glutathione redox status by endosulfan.

The oxidant stress-inducing effects of endosulfan, a chlorinated hydrocarbon insecticide of the cyclodiene group, have been examined following ig administration of single and repeated doses. A single dose of 30 mg/kg (approximately 30% LD50) endosulfan significantly (p < 0.001) increased the TBARS and, hence, the lipid peroxidation in cerebral and hepatic tissues of rats. Administration of endosulfan with doses of 10 or 15 mg/kg/d for 5 d has also induced lipid peroxidation significantly (p < 0.05). The same doses caused a significant alteration in glutathione redox status of cerebral and hepatic tissues, where total glutathione and oxidized glutathione were measured by an enzymatic cycling procedure. Selenium levels were also determined and compared with controls. With repeated doses, oxidant stress was more pronounced in cerebral tissue, where endosulfan shows a GABA-antagonistic activity. The possible relationship between the neurotoxicity of endosulfan and its oxidant stress-inducing effect was discussed.

Animals↗
PubMed2001

The protective role of selenium on genetic damage and on cancer.

Collectively, results from epidemiologic studies, laboratory bioassays, and human clinical intervention trials clearly support a protective role of selenium against cancer development. Several hypotheses have been proposed to explain these observations. Increased genomic instability, either inherent or induced by exogenous agents (mutagens or carcinogens), has been considered as a primary event leading to neoplastic transformation. This report deals specifically with the evidence for a role of selenium in the inhibition of carcinogen-induced covalent DNA adduct formation and retardation of oxidative damage to DNA, lipids and proteins, and for modulating cellular and molecular events that are critical in cell growth inhibition and in the multi-step carcinogenesis process. At present, the bulk of our knowledge on the role of selenium on genetic stability is based primarily on animal data and from studies conducted in in vitro systems. Studies performed in vitro showed that the dose and form of selenium compounds are critical factors with regard to cellular responses. Inorganic (at doses up to 10microM) and organic selenium compounds (at doses equal to or greater than 10microM) elicit distinctly different cellular responses. The recommended daily allowance (RDA) is 50-70 microgramSe per day for healthy adults; with 40 microgramSe as minimum requirement. Less than 11 microgramSe will definitely put people at risk of deficiency that would be expected to cause genetic damage. Daily doses of 100-200 microgramSe inhibited genetic damage and cancer development in humans. About 400 microgramSe per day is considered an upper limit. Clearly, doses above the RDA are needed to inhibit genetic damage and cancer. However, it has been hypothesized that the intake of excessive doses of selenium may cause oxidative damage, leading to genomic instability. The use of a cocktail consisting of selenium, and other vitamins and minerals appears to be a promising approach to inhibit genetic damage and the development of cancer. It is the author's recommendation that development of mechanism-based hypotheses that can be tested in pilot studies in different populations prior to a large-scale clinical trial in humans, is of paramount importance in order to better understand the role of selenium on genetic stability and cancer.

Animals↗
PubMed2003

Oxidant stress enhances Lyso-PAF-AcT activity by modifying phospholipase D and phosphatidic acid in aortic endothelial cells.

Oxidant stress, as a consequence of selenium (Se) deficiency, alters production of vasoactive compounds including platelet-activating factor (PAF). Recent studies report that enhanced PAF production during Se deficiency is a consequence of increased lyso-PAF:acetyl-coenzyme A acetyltransferase (Lyso-PAF-AcT) activity. To elucidate the mechanism behind increased Lyso-PAF-AcT activity during oxidant stress, phospholipase D (PLD) activity and phosphatidic acid (PA) production were examined. Increased PLD activity and PA production were exhibited in bovine aortic endothelial cells using a Se-deficient model of oxidant stress. The direct effects of PLD and PA on Lyso-PAF-AcT activity were assessed using selective inhibitors and repletion experiments. Following the inhibition of PLD and addition of exogenous PA, Lyso-PAF-AcT activity significantly decreased and increased, respectively. Therefore, Se deficiency enhances Lyso-PAF-AcT activity in part by modifying PLD and PA. This suggests a novel link between Se status and PAF production, providing potential upstream therapeutic targets for PAF regulation under conditions of oxidant stress.

Acetyltransferases↗
PubMed2004

[Spectrophotometry determination of trace selenium(IV) in Chinese herbal medicine by catalytic kinetics. I. RDB and potassium bromate].

Trace Se(IV) can catalyze the discolouring oxidizing reaction of RDB with potassium bromate in nitric acid medium, and the conditions of kinetics has been studied in detail. A new method of kinetics spectrophotometry for determination of trace (IV) is established. The sensitivity of the method is 0.905 microg x L(-1). The range of measurement is 0-9.6 microg x L(-1). The method has been used for determining trace Se(IV) in Chinese herbal medicine with satisfactory results.

Bromates↗
PubMed1983

Macrophage, lymphocyte and chronic inflammatory responses in selenium deficient rodents. Association with decreased glutathione peroxidase activity.

The influence of a selenium deficient diet in mice and rats has been studied on glutathione peroxidase (GSH-Px) and secretory activities of peritoneal macrophages, mitogenesis of spleen cells and adjuvant arthritis. Macrophage GSH-Px activity was significantly reduced from 9 weeks on the selenium deficient diet. This reduction was associated with enhanced macrophage H2O2 release on zymosan stimulation after 12 weeks on the diet, a similar trend in chemiluminescence and reduced mitogenesis of spleen cell cultures to T and B cell mitogens after 8 weeks on the diet. Macrophage beta-glucuronidase release was not significantly altered. Phorbol myristic acetate induced macrophage H2O2 generation was reduced by selenium deficiency, possibly due to increased cellular damage. Adjuvant arthritis of rats was significantly enhanced after 6 and 12 weeks on the selenium deficient diet. The enhanced release of H2O2 by macrophages after zymosan stimulation can be directly attributable to loss of GSH-Px activity leading to reduced peroxide breakdown. Peroxide-mediated cell injury would also account for the reduction in lymphocyte mitogenesis and enhancement of adjuvant arthritis. These data provide support for a role of selenium in immune and inflammatory responses.

Animals↗
PubMed2003

Skeletal muscle disorders associated with selenium deficiency in humans.

Skeletal muscle disorders manifested by muscle pain, fatigue, proximal weakness, and serum creatine kinase (CK) elevation have been reported in patients with selenium deficiency. The object of this report was to review the conditions in which selenium deficiency is associated with human skeletal muscle disorders and to evaluate the importance of mitochondrial alterations in these disorders. A systematic literature review using the Medline database and Cochrane Library provided 38 relevant articles. The main conditions associated with selenium deficiency fell into three categories: (1) insufficient selenium intake in low soil-selenium areas; (2) parenteral or enteral nutrition, or malabsorption; and (3) chronic conditions associated with oxidative stress, such as chronic alcohol abuse and human immunodeficiency virus (HIV) infection. In low soil-selenium areas, reversibility of muscle symptoms was similar after selenium supplementation and placebo administration, suggesting a role for other factors in the development of disease. In parenteral or enteral nutrition, or malabsorption, muscle symptoms improved after selenium supplementation in 18 of 19 patients (median delay: 4 weeks). The reason that only a minority of selenium-deficient patients present with skeletal muscle disorders is unclear and is possibly related to cofactors, such as viral infections and drugs. Prospective studies of selenium-deficient myopathies would be useful in critically ill patients, alcohol abusers, and HIV-infected patients.

Adult↗
PubMed1996

Role of lipid peroxidation, trace elements and anti-oxidant enzymes in chronic renal disease patients.

Plasma Selenium (Se), Zinc (Zn), Copper (Cu) and Aluminium (Al) levels, red blood cell vitamin E and antioxidant enzymes, glutathione peroxidase (GPX) and catalase activity were studied in 54 patients with renal diseases of different levels of kidney dysfunction. Group I (serum creatinine < 2 mg/dl), Group II (serum creatinine 2-4 mg/dl), Group III (serum creatinine 4.1-8 mg/dl), Group IV (serum creatinine 8.1-12 mg/dl) Group V (serum creatinine > 12 mg/dl); thirty two healthy subjects are controls. Plasma Zn (ug/L) and red blood cell vitamin E (ug/ml PRC) were decreased more significantly than controls (1348.59 +/- 43.72 vs 1318.89 +/- 45.62, and 3.38 +/- 0.45 vs 2.23 +/- 0.52) while plasma Selenium and Copper are within normal ranges. Plasma GSH-PX and catalase activity (IU/ml PRC) were also decreased (28.26 +/- 9.01 vs 20.48 +/- 6.79 and 7.54 +/- 1.91 vs 6.52 +/- 2.31) more significantly than controls. Lipid peroxidation products, plasma (umol/L) and urine malonaldehyde (MDA, umol/Ccr) were elevated (7.29 +/- 3.39 vs 92.94 +/- 61.66, and 32.08 +/- 24.60 vs 246.14 +/- 325.66) significantly (p < 0.0001). The lipid peroxidation abnormalities were seen in patients with normal renal function, which supports the role of oxidative stress early in the course of renal disease. Urine ammonia per GFR was also increased as well as urine B2m and NAG. There was no correlation between lipid peroxidation product (MDA) and any of the antioxidant enzymes, vitamin E, urine NH3, B2m, protein or NAG except urine ammonia and MDA per nephron which correlate with severity of kidney dysfunction which confirmed the role of complex processes in the progression of chronic renal failure. The early intervention to decrease oxygen consumption either by dietary protein restriction antioxidants such as vitamin E supplement or calcium channels blockers may be of value in preserving renal function in the setting of chronic renal failure.

Chronic Disease↗