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PubMed2004

Metabolism of selenomethionine by rainbow trout (Oncorhynchus mykiss) embryos can generate oxidative stress.

Although selenium is required by vertebrates, toxicity can arise at concentrations only slightly greater than those they require. The toxicity of Se is thought to arise from its ability to substitute for sulfur during the assembly of proteins. However, recent studies also indicate that some forms of selenium are capable of generating oxidative stress in an in vitro test system that includes glutathione. L-Selenomethionine, the predominant form of selenium in the eggs of oviparous vertebrates, does not generate oxidative radicals in this system, but lesions consistent with oxidative stress have been identified in fish and birds with high concentrations of Se. Here we report on the ability of rainbow trout embryos to transform L-Selenomethionine to a form capable of producing a superoxide radical. Oxidative stress appears to be generated by methioninase enzyme activity in the embryos that liberates methylselenol from l-Selenomethionine. Methylselenol redox cycles in the presence of glutathione producing superoxide and likely accounts for oxidative lesions present in fish and birds environmentally exposed to excessive loads of selenomethionine.

Animals↗
PubMed2002

One-electron oxidation of plasmid DNA by selenium(V) species.

PURPOSE: To employ the gamma-radiation-generated selenium(V) one-electron-oxidizing agent SeO3*- for the preparation of guanyl radicals in plasmid DNA, and to compare the behaviour of this reagent with that of other similarly reactive oxidant species. MATERIALS AND METHODS: Plasmid DNA in aerobic aqueous solution was irradiated with 137Cs gamma-rays (662 keV). The solutions also contained up to 4x10(-2) mol x dm(-3) sodium selenate (Na2SeO4) and/or up to 10(-1) mol x dm(-3) sodium biselenite (NaHSeO3), as well as auxiliary scavengers such as DMSO or glycerol. In some cases, reducing agents such as ferrocyanide were also present. After irradiation, the plasmid was incubated with the Escherichia coli base excision-repair endonuclease formamidopyrimidine-DNA N-glycosylase (FPG). These treatments produced strand breaks in the plasmid. The yields of these strand breaks were quantified by agarose gel electrophoresis. RESULTS: In general, gamma-irradiation produced single-strand breaks (SSB) in plasmid DNA. Subsequent incubation with the endonuclease FPG increased the SSB yield by a factor of 2-100-fold. The smallest effects of FPG were observed when only DMSO or glycerol were present during irradiation. FPG incubation produced significantly larger increases in the SSB yield after gamma-irradiation in the additional presence of selenate and/or biselenite. The largest effect of FPG was observed after gamma-irradiation in the presence of 10(-2) mol x dm(-3) sodium selenate and 10(-1) mol x dm(-3) glycerol. This was indicative of extensive oxidative damage to the plasmid under these conditions and provided evidence for guanine oxidation mediated by SeO3*-. The large effect of FPG was strongly attenuated by the addition of reducing agents such as ferrocyanide. The observations suggest that these reducing agents exert their effects through the reduction of an intermediate guanyl radical. CONCLUSION: By comparing the yields of breaks produced after gamma-irradiation under a range of conditions, it is possible to formulate a reaction scheme that describes the chemical reactions responsible for the formation of strand breaks and FPG-sensitive sites. By applying this scheme to the data, we can quantify rate constants for the reduction of DNA guanyl radicals by reducing agents. This reaction is of particular interest to radiation biology because it is the equivalent of the repair of DNA damage by the direct effect of ionizing radiation.

Binding Sites↗
PubMed1997

Effect of diet induced hypercholesterolemia and selenium supplementation on nitric oxide synthase activity.

The aim of the present study was to examine the activity of nitric oxide synthase (NOS, EC 1.14.23) in plasma of high fat diet (HFD, 2% cholesterol and 100 g table butter/kg diet) and HFD + selenium (Se, 1 ppm as sodium selenite) fed rabbits for three months. Significant increase in the serum cholesterol and triglyceride levels in HFD fed group was observed. The activity of NOS also increased very significantly. However in Se supplemented animals, there was a significant reduction in serum cholesterol as well as in plasma NOS activity relative to HFD fed animals. It is concluded that the protective effect of Se on HFD induced NOS activity acts probably through its antioxidant/inhibitory action.

Animals↗
PubMedDate not supplied

The reaction of ebselen with peroxynitrite.

Ebselen, 2-phenyl-1,2-benzisoselenazol-3(2H)-one, rapidly reacts with peroxynitrite, the rate constant being of the order of 10(6) M-1 s-1; the reaction yields the selenoxide of the parent molecule, 2-phenyl-1,2-benzisoselenazol-3(2H)-one 1-oxide, as the sole selenium-containing product; a stoichiometry of 1 mol of ebselen reacted and of the selenoxide formed per mole of peroxynitrite was observed. The reaction was studied in detail at neutral and alkaline pH (pH 10-11). It also proceeds at acidic pH where peroxynitrous acid (ONOOH) is predominant, the yield of the selenoxide being lower because peroxynitrous acid (pKa = 6.8) decays rapidly. Reduction of the selenoxide in cells to regenerate ebselen would allow for a sustained defense against peroxynitrite. This novel reaction constitutes a potential cellular defense line against peroxynitrite, one of the important reactive species in inflammatory processes.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2002

Semisynthesis of new sarcophine derivatives with chemopreventive activity.

The natural cembranolide sarcophine (3) and its lactone ring-opened analogue (10) were oxidized using selenium dioxide under different reaction temperatures to prepare hydroxylated derivatives. Nine new compounds were obtained, six of them targeted hydroxylated derivatives. The determination of regio- and stereochemistry as well as the mechanistic considerations on the selectivity observed in these reactions are discussed on the basis of 2D NMR and molecular modeling. In preliminary in vitro tests on inhibition of EBV-EA activation, compounds 10 and 12-15 have shown higher activity than the known chemopreventive agent sarcophytol A.

4-Butyrolactone↗
PubMed2001

Selenium-deficient diet induces renal oxidative stress and injury via TGF-beta1 in normal and diabetic rats.

BACKGROUND: Oxidative stress has been implicated in the pathogenesis of diabetic nephropathy. Although glucose itself can initiate oxidative stress, deficiency of essential trace elements such as selenium (Se) may exacerbate this oxidative stress in diabetic rats. The mechanism by which Se deficiency causes oxidative stress and renal injury is not completely understood. This study tested the hypothesis that Se deficiency induces renal oxidative stress and renal injury via transforming growth factor-beta1 (TGF-beta1). METHODS: Fifty-four male Wistar rats were used. Diabetes was induced in 27 rats by streptozotocin, and the other 27 rats received buffer only. Ten weeks after induction of diabetes, both normal and diabetic rats were killed, their kidneys removed, and glomeruli were isolated. Glomeruli from normal and diabetic rats were incubated in the presence of TGF-beta1 alone or its neutralizing antibody. Antioxidant enzyme (Cu-Zn) superoxide dismutase (Cu-Zn SOD), catalase, and glutathione peroxidase (GSH-Px) activities; total glutathione; and lipid peroxidation were determined. For Se studies, 15 normal and 15 diabetic rats were divided into groups of five each and fed either a regular, Se-deficient, or Se-supplemented diet one week after induction of diabetes. Ten weeks after feeding these diets, rats were killed and glomeruli were isolated. Oxidative stress was examined by determining the mRNA expressions for antioxidant enzymes and also for TGF-beta1. Plasma glucose and albuminuria were determined. Histology of the kidney and interlobular artery was evaluated by light microscopy. RESULTS: In vitro studies showed that TGF-beta1 significantly reduced glomerular catalase and GSH-Px activities as well as total glutathione levels with an increase in lipid peroxidation in both normal and diabetic rats. Antibody to TGF-beta abrogated these changes. There was no effect of TGF-beta1 on Cu-Zn SOD. Like TGF-beta1, a Se-deficient diet caused a significant decrease in glomerular mRNA expression for Cu-Zn SOD, catalase, and GSH-Px, but a significant increase in TGF-beta1 mRNA expression. Also, a Se-deficient diet caused an increase in albuminuria, glomerular sclerosis, and plasma glucose levels in both normal and diabetic rats. The deficient diet caused a decrease in the lumen size of the interlobular artery. Se supplementation to diabetic rats up-regulated mRNA expression for antioxidant enzymes, and significantly reduced but did not normalize that of TGF-beta1. Glomerular sclerosis was normalized and the interlobular artery lumen size was greatly enlarged in diabetic rats by Se supplementation. Also, the tubulointerstitium was preserved by Se supplementation in diabetic rats. CONCLUSIONS: The data show that TGF-beta1 is a pro-oxidant and Se deficiency increases oxidative stress via this growth factor. In addition, Se deficiency may simulate hyperglycemic conditions. Se supplementation to diabetic rats prevents not only oxidative stress but renal structural injury, as well.

Animals↗
PubMed2001

Effects of selected polychlorinated biphenyl (PCB) congeners on hepatic glutathione, glutathione-related enzymes, and selenium status: implications for oxidative stress.

Polychlorinated biphenyls (PCBs) induce drug metabolism that may lead to the bioactivation of PCBs themselves or alternatively may lead to oxidative events within the cell. The goal of the present study was to determine the influence of congeneric PCBs, selected as substrates for or inducers of drug metabolism, upon hepatic glutathione, glutathione-related enzymes, and selenium status. Male and female Sprague-Dawley rats received two i.p. injections per week of PCB 3 (4-chlorobiphenyl), PCB 28 (2,4,4'-trichlorobiphenyl), PCB 38 (3,4,5-trichlorobiphenyl), PCB 77 (3,3',4,4'-tetrachlorobiphenyl), PCB 153 (2,2',4,4',5,5'-hexachlorobiphenyl), or both PCBs 77 and 153 (100 micromol/kg/injection) and were killed at the end of 1, 2, or 3 weeks. Whole liver homogenates, hepatic cytosol, and microsomes were prepared. Both glutathione reductase and glutathione transferase activities were increased significantly in both male and female rats receiving PCB 77, an aryl hydrocarbon receptor agonist, as well as in those receiving both PCBs 77 and 153. No significant trend was observed in the levels of hepatic total glutathione. PCB 77 treatment decreased hepatic selenium-dependent glutathione peroxidase (SeGPX) activity in both male and female rats significantly. This decrease in activity following PCB 77 treatment was accompanied by a decrease in the cytosolic selenium-dependent glutathione peroxidase gene (GSPx1) transcript, as well as a decrease in hepatic total selenium levels. These data support the concept that exposure to the coplanar PCB 77 suppresses, via gene regulatory mechanisms, the cellular antioxidant enzyme SeGPX and that this decrease involves selenium. Lower halogenated PCBs that may be bioactivated to reactive oxygen species (ROS)-producing metabolites, and higher halogenated PCBs that are not Ah receptor agonists, were inactive.

Analysis of Variance↗
PubMed2004

Experimental and theoretical investigations of structural trends for selenium(IV) imides and oxides: X-ray structure of Se3(NAd)2.

The thermal decomposition of Se(NAd)(2) (Ad = 1-adamantyl) in THF was monitored by (77)Se NMR and shown to give the novel cyclic selenium imide Se(3)(NAd)(2) as one of the products. An X-ray structural determination showed that Se(3)(NAd)(2) is a puckered five-membered ring with d(Se-Se) = 2.404(1) A and |d(Se-N)| = 1.873(4) A. On the basis of (77)Se NMR data, other decomposition products include the six-membered ring Se(3)(NAd)(3), and the four-membered rings AdNSe(micro-NAd)(2)SeO and OSe(micro-NAd)(2)SeO. The energies for the cyclodimerization of E(NR)(2) and RNEO (E = S, Se; R = H, Me, (t)Bu, SiMe(3)), and the cycloaddition reactions of RNSeO with E(NR)(2), RNSO(2) with Se(NR)(2), and S(NR)(2) with Se(NR)(2) have been calculated at MP2, CCSD, and CCSD(T) levels of theory using the cc-pVDZ basis sets and B3PW91/6-31G* optimized geometries. Sulfur(IV) and selenium(IV) diimide monomers are predicted to be stable, the sole exception being Se(NSiMe(3))(2) that shows a tendency toward cyclodimerization. The cyclodimerization energy for RNSeO and the cycloaddition reaction energies of RNSeO with Se(NR)(2) as well as that of RNSO(2) with Se(NR)(2) are negative, consistent with the observed formation of OSe(micro-N(t)Bu)(2)SeO, OSe(micro-N(t)Bu)(2)SeN(t)Bu, and O(2)S(micro-N(t)Bu)(2)SeN(t)Bu, respectively. Cycloaddition is unlikely when one of the reactants is a sulfur(IV) diimide.

Journal Article↗
PubMed2000

A method for measuring disulfide reduction by cultured mammalian cells: relative contributions of glutathione-dependent and glutathione-independent mechanisms.

A method is described for measuring bioreduction of hydroxyethyl disulfide (HEDS) or alpha-lipoate by human A549 lung, MCF7 mammary, and DU145 prostate carcinomas as well as rodent tumor cells in vitro. Reduction of HEDS or alpha-lipoate was measured by removing aliquots of the glucose-containing media and measuring the reduced thiol with DTNB (Ellman's reagent). Addition of DTNB to cells followed by disulfide addition directly measures the formation of newly reduced thiol. A549 cells exhibit the highest capacity to reduce alpha-lipoate, while Q7 rat hepatoma cells show the highest rate of HEDS reduction. Millimolar quantities of reduced thiol are produced for both substrates. Oxidized dithiothreitol and cystamine were reduced to a lesser degree. DTNB, glutathione disulfide, and cystine were only marginally reduced by the cell cultures. Glucose-6-phosphate deficient CHO cells (E89) do not reduce alpha-lipoate and reduce HEDS at a much slower rate compared to wild-type CHO-K1 cells. Depletion of glutathione prevents the reduction of HEDS. The depletion of glutathione inhibited reduction of alpha-lipoate by 25% and HEDS by 50% in A549 cells, while GSH depletion did not inhibit alpha-lipoate reduction in Q7 cells but completely blocked HEDS reduction. These data suggest that the relative participation of the thioltransferase (glutaredoxin) and thioredoxin systems in overall cellular disulfide reduction is cell line specific. The effects of various inhibitors of the thiol-disulfide oxidoreductase enzymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenylarsine oxide) support this conclusion.

Animals↗
PubMed2004

Selenium supplementation and ischemia-reperfusion injury in rats.

Cardiac ischemia--reperfusion injury results in oxidative stress and poor physiological recovery. This study examined the amount of lipid and protein oxidation during ischemia-reperfusion to assess the degree of oxidative stress. Selenium supplementation was used to alter the antioxidant status of rats and the recovery of myocardial function post ischemia-reperfusion was investigated. Male Wistar rats were fed diets containing 0, 50, and 1000 microg/kg sodium selenite for 5 weeks, whilst controls received normal rat food containing 240 microg/kg selenium. Langendorff-perfused hearts were subjected to 22.5 min global ischemia and 45 min reperfusion, with functional recovery assessed. Heart tissues were assayed for the presence of lipid peroxides and protein carbonyls and correlated to cardiac recovery. Following ischemia and reperfusion there was a significant increase in both protein oxidation and lipid peroxidation. Hearts from selenium-deficient animals demonstrated higher levels of both protein carbonyls and lipid peroxides and were more susceptible to ischemia-reperfusion injury when compared to controls (38% versus 47% recovery of rate pressure product (RPP)). Selenium supplementation lowered the levels of protein carbonyls and lipid peroxides and resulted in improved recovery of cardiac function post ischemia-reperfusion (57% recovery of RPP). These data suggest that selenium supplementation may provide an effective method for reducing oxidative damage post cardiac ischemia-reperfusion.

Animals↗
PubMed1998

Plasma levels of antioxidant vitamins, selenium, total sulfhydryl groups and oxidative products in ischemic-stroke patients as compared to matched controls in Taiwan.

The possible involvement of oxidative damage and antioxidant protection has been suggested in the pathogenesis of stroke which is the second-leading cause of death in Taiwan. In this study we investigated the relationship between ischemic stroke and plasma status of antioxidants and oxidative products. Plasma levels of vitamin A, alpha-tocopherol, carotenoids, selenium (Se), total SH groups (T-SH), thiobarbituric acid-reactive substances (TBARS) and protein carbonyl, a marker of protein damage, were determined in ischemic-stroke patients (n = 36, blood sampled within 24 hrs after the clinical event) in comparison with 21 matched controls. The cholesterol-adjusted carotenoids and vitamin E were significantly lower (P < 0.05) in the plasma of ischemic-stroke patients than those of the controls. TBARS were higher (P < 0.05) in the patients than in the controls but Se, T-SH and protein carbonyls were not significantly different between the two groups. Separation of the patients into small-artery ischemic stroke (SAIS, n = 17) and large-artery ischemic stroke (LAIS, n = 19) groups revealed that both carotenoids/cholesterol and vitamin E/cholesterol ratios were significantly lower in both LAIS and SAIS groups than the controls (n = 21) while vitamin A/cholesterol was not different among the three groups. TBARS were only significantly higher in the LAIS group. The results demonstrated that, within 24 hrs after the clinical event, the acute-ischemic stroke patients had lowered levels of cholesterol-adjusted carotenoids and alpha-tocopherol but elevated levels of TBARS in the plasma as compared to the matched controls. It remains to be resolved as to whether enhanced lipid peroxidation is a cause or a result of lowered antioxidants in ischemic stroke.

Adult↗
PubMed2002

Blood selenium concentrations and enzyme activities related to glutathione metabolism in wild emperor geese.

In 1998, we collected blood samples from 63 emperor geese (Chen canagica) on their breeding grounds on the Yukon-Kuskokwim Delta (YKD) in western Alaska, USA. We studied the relationship between selenium concentrations in whole blood and the activities of glutathione peroxidase and glutathione reductase in plasma. Experimental studies have shown that plasma activities of these enzymes are useful biomarkers of selenium-induced oxidative stress, but little information is available on their relationship to selenium in the blood of wild birds. Adult female emperor geese incubating their eggs in mid-June had a higher mean concentration of selenium in their blood and a greater activity of glutathione peroxidase in their plasma than adult geese or goslings that were sampled during the adult flight feather-molting period in late July and early August. Glutathione peroxidase activity was positively correlated with the concentration of selenium in the blood of emperor geese, and the rate of increase relative to selenium was greater in goslings than in adults. The activity of glutathione reductase was greatest in the plasma of goslings and was greater in molting adults than incubating females but was not significantly correlated with selenium in the blood of adults or goslings. Incubating female emperor geese had high selenium concentrations in their blood, accompanied by increased glutathione peroxidase activity consistent with early oxidative stress. These findings indicate that further study of the effects of selenium exposure, particularly on reproductive success, is warranted in this species.

Alaska↗
PubMed2005

Protection of mitochondrial integrity from oxidative stress by selenium-containing glutathione transferase.

The antioxidant activity of a novel artificial glutathione peroxidase-like enzyme, selenium-containing glutathione 5-transferase from Lucilia cuprina (seleno-LuGST1-1), was studied by using a ferrous sulfate/ascorbate-induced mitochondrial damage model system. Swelling of mitochondria, lipid peroxidation, and cytochrome-c oxidase activity were selected to evaluate the preservation of mitochondrial integrity in this system. Seleno-LuGST1-1 could effectively protect the mitochondria against oxidative damage in a dose-dependent manner and exhibited both higher catalytic activity and greater antioxidant ability than the classic mimic, 2-phenyl-1,2-benziososelenazol-3(2H)-one (Ebselen). This novel artificial biocatalyst therefore may have great potential for pharmacologic application in the treatment of reactive oxygen species-related diseases.

Animals↗
PubMed1992

Inhibition of the biosynthesis of N-acetylneuraminic acid by metal ions and selenium in vitro.

In liver homogenate the biosynthesis of N-acetylneuraminic acid using N-acetylglucosamine as precursor can be followed stepwise by applying different chromatographic procedures. In this cell-free system 16 metal ions (Zn2+, Mn2+, La3+, Co2+, Cu2+, Hg2+, VO3-, Pb2+, Ce3+, Cd2+, Fe2+, Fe3+, Al3+, Sn2+, Cs+ and Li+) and the selenium compounds, selenium(IV) oxide and sodium selenite, have been checked with respect to their ability to influence a single or possibly several steps of the biosynthesis of N-acetylneuraminic acid. It could be shown that the following enzymes are sensitive to these metal ions (usually applied at a concentration of 1 mmol l-1): N-acetylglucosamine kinase (inhibited by Zn2+ and vandate), UDP-N-acetylglucosamine-2'-epimerase (inhibited by Zn2+, Co2+, Cu2+, Hg2+, VO3-, Pb2+, Cd2+, Fe3+, Cs+, Li+, selenium(IV) oxide and selenite), and N-acetylmannosamine kinase (inhibited by Zn2+, Cu2+, Cd2+ and Co2+). Dose dependent measurements have shown that Zn2+, Cu2+ and selenite are more efficient inhibitors of UDP-N-acetylglucosamine-2'-epimerase than vanadate. As for the N-acetylmannosamine kinase inhibition, a decreasing inhibitory effect exists in the following order Zn2+, Cd2+, Co2+ and Cu2+. In contrast, La3+, Al3+ and Mn2+ (1 mmol l-1) did not interfere with the biosynthesis of N-acetylneuraminic acid. Thus, the conclusion that the inhibitory effect of the metal ions investigated cannot be regarded as simply unspecific is justified.

Acetylglucosamine↗