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PubMed1986

Menadione (2-methyl-1,4-naphthoquinone)-induced Ca2+ release from rat-liver mitochondria is caused by NAD(P)H oxidation.

Incubation of rat-liver mitochondria with menadione in the presence of succinate and rotenone resulted in rapid glutathione and NAD(P)H oxidation followed by Ca2+ release and mitochondrial swelling. Ca2+ release, NAD(P)H oxidation and mitochondrial swelling, were also observed in mitochondria from selenium-deficient rats. Glutathione was only slowly oxidized, suggesting that glutathione oxidation, and subsequent NAD(P)H oxidation via the glutathione peroxidase-glutathione reductase system were not required for Ca2+ release by menadione. Isocitrate prevented and reversed Ca2+ release dose-dependently but dicoumarol had no effect indicating that NADH-ubiquinone oxidoreductase and not DT-diaphorase was responsible for NAD(P)H oxidation. Superoxide anion radical was formed by cyanide-resistant respiration, suggesting that menadione undergoes a one-electron reduction to an autoxidizable semiquinone radical by NADH-ubiquinone oxidoreductase. The inability of menadione to oxidize glutathione in selenium-deficient mitochondria indicates that the metabolism of the superoxide dismutation product, H2O2, by glutathione peroxidase was probably responsible for the glutathione oxidation in selenium-replete mitochondria.

Animals↗
PubMed2004

Novel chemiluminescence-inducing cocktails, part I: the role in light emission of combinations of luminal with SIN-1, selenite, albumin, glucose oxidase and Co2+.

It is known that many agents influence the capacity of cells to produce reactive oxygen species. However, assaying these agents, both those that stimulate and those that inhibit reactive oxygen production, can be complicated and time consuming. Here, a method is described in which two different cocktails are employed to stimulate luminol-dependent chemiluminescence (LDCL). These cocktails are comprised of luminol, with either sodium selenite [IV] (SEL) or tellurite [IV] (TEL) (where IV and VI refer to the 4+ or 6+ oxidation state of selenium or tellurium salts, respectively), morpholinosidonimine (SIN-1), serum albumin and Co(2+), called the SIN-1a (with selenite) and SIN1b (with tellurite) cocktails, respectively; or luminol with glucose oxidase (GO), sodium selenite [IV] and Co(2+), called the GO cocktail. The cocktails functioned best in Hank's balanced salt solution (HBSS) containing 1% glucose at pH 7.4, incubated at approximately 22 degrees C. Within 30-60 s there was a burst of luminescence, which lasted for 7-10 min. In 100% ethanol, the SIN-1 cocktails also generated LDCL to 70% of that produced in HBSS. Neither selenite [VI], seleno-cystine, seleno-methionine, nor the selenium-containing drug, ebselen, could replace SEL. Moreover, the effects of the NO-donor, SIN-1, could not be replicated by the oxyradical generators, xanthine-xanthine oxidase or hypochlorous acid. Only low levels of luminescence were generated by combinations of the peroxyl radical generator, 2,2'-azobis-2-amidinopropane dihydrochloride (AAPH) with either SEL or TEL. It is suggested that light emission induced by the SIN1 cocktail results from the oxidation of SEL [IV] to the [VI] state, possibly due to the generation of mixtures of superoxide, peroxide, peroxynitrite and also of unidentified oxidant species, catalyzed by CoCo(2+). However, the involvement of hydroxyl radicals in LDCL could not be confirmed by use of either dimethyl thiourea or by electron spin resonance (ESR). LDCL induced by the two cocktails is strongly reduced by phosphates, EDTA, deferoxamine, CuCo(2+), MnCo(2+), as well as by the "classical" antioxidants superoxide dismutase (SOD), ascorbate, vitamin E, uric acid or thiols. It is suggested that these chemiluminescence cocktail systems can be used to determine the total anti-oxidant capacities of biological fluids and commercially available anti-oxidants.

Antioxidants↗
PubMed2003

Effects of salinity on the uptake, biotransformation, and toxicity of dietary seleno-L-methionine to rainbow trout.

Selenium (Se) is an element that has been of environmental concern in aquatic systems that drain arid regions heavily used for agricultural purposes. As hypersaline conditions are associated with these ecosystems, this study examined the effect of hypersaline water on the uptake, biotransformation, and toxicity of seleno-L-methionine (SeMe) in juvenile rainbow trout. Fish were acclimated for 5 days to four different salinity regimes (0.5, 6.3, 11.9, 16.8 deciSiemens (dS/m) per meter. To mimic arid agricultural runoff solutes, the water was reconstituted with ions found in drainage water of the San Joaquin River in California. Following 7 days of dietary exposure to 180 mg/kg SeMe, mortality, as well as hepatic selenium concentrations and reduced:oxidized glutathione ratios were measured. Hypersaline conditions protected fish from dietary SeMe toxicity. Fish exposed to 0.5 dS/m water experienced 100% lethality in 2.5 days, whereas fish acclimated to 16.8 dS/m water-only experienced 16.7% mortality, which took 5-7 days to occur. There were no significant differences in hepatic selenium concentrations, but diminishment of reduced glutathione:oxidized glutathione (GSH:GSSG) ratios was observed in SeMe-treated fish held in 0.5 dS/m water. SeMe inhibited flavin-containing monoxygenase catalyzed trimethylamine oxidase activity, but salinity failed to induce expression in trout, indicating an oxygenation of organoselenides may play a minor role in SeMe toxicity.

Animals↗
PubMed1995

Subcellular distribution of selenium during uptake and its influence on mitochondrial oxidations in germinating Vigna radiata L.

The metabolic significance of Se in plants is not well documented, though the presence of many selenoenzymes in bacteria and the essentiality of Se in higher animals is established. Since germination is an active process in plant growth and metabolism, the effect of Se was investigated in germinating Vigna radiata L, a nonaccumulating Se-deficient legume. Growth and protein were enhanced in seedlings supplemented with selenium (Se) as sodium selenite in the medium up to 1 microgram/mL. The pattern of uptake of 75Se in the differentiating tissues and the subcellular distribution were investigated. The percentage of incorporation of 75Se was greater in the mitochondria at the lowest level (0.5 micrograms/mL) of Se supplementation compared to higher levels of Se exposure. Proteins precipitated from the postmitochondrial supernatant fractions, when separated by means of polyacrylamide gel electrophoresis (PAGE), indicated a major selenoprotein in the seedlings germinated at 2.0 micrograms/mL Se. In seedlings grown with supplemented Se, enhanced respiratory control ratio and succinate dehydrogenase activity were observed in the mitochondria of tissues, indicative of a role for Se in mitochondrial membrane functions.

Cotyledon↗
PubMed1988

Vitamin E and selenium regulate balance between beta-adrenergic and muscarinic responses in rat lungs.

The effects of hydrogen peroxide on the beta-adrenergic and muscarinic responses of the rat trachea muscle were studied in vitro, after feeding rats, for 6 weeks, either a diet deficient in vitamin E and selenium or a control diet. In the control situation after incubation with 1 mM hydrogen peroxide for 30 min, a reduction of the maximal response to methacholine of 39% occurred whereas no pD2 shift could be demonstrated. Moreover, no response to isoprenaline after precontraction with 3 x 10(-7) M methacholine was left. In the deficient situation, we found a reduction to 64% of the response to methacholine after incubation with 1 mM hydrogen peroxide. Again isoprenaline became inactive, i.e. no relaxation with isoprenaline was observed after precontraction with 3 x 10(-7) M methacholine. We therefore conclude that vitamin E and selenium protect against oxidative stress in lung tissue and thus regulate the (patho-) physiological balance between adrenergic and muscarinic responses.

Animals↗
PubMed2001

Evidence for the presence of phospholipid hydroperoxide glutathione peroxidase in human platelets: implications for its involvement in the regulatory network of the 12-lipoxygenase pathway of arachidonic acid metabolism.

The 12-lipoxygenase pathway of arachidonic acid metabolism in platelets and other cells is bifurcated into a reduction route yielding 12-hydroxyeicosatetraenoic acid (12-HETE) and an isomerization route forming hepoxilins. Here we show for the first time the presence of phospholipid hydroperoxide glutathione peroxidase (PHGPx) protein and its activity in platelets. The ratio of the activity of PHGPx to that of cytosolic glutathione peroxidase (GPx-1) was consistently found to be approx. 1:60 in platelets and UT7 megakaryoblasts. Moreover, short-lived PHGPx mRNA was detected in megakaryocytes but not in platelets. Carboxymethylation of selenium-containing glutathione peroxidases by iodoacetate, which results in the inactivation of PHGPx and GPx-1 without inhibition of 12-lipoxygenase, markedly altered the pattern of arachidonic acid metabolism in human platelets. Whereas the formation of 12-HETE was inhibited by 80%, a concomitant accumulation of 12-hydroperoxyeicosatetraenoic acid (12-HpETE) by two orders of magnitude as well as the formation of hepoxilins A(3) and B(3) were observed. The formation of hepoxilins also occurred when 12-HpETE was added to untreated platelets. In selenium-deficient UT7 cells, which were devoid of GPx-1 but not of PHGPx, the reduction of 12-HPETE was retained, albeit with a lower rate than in control cells containing GPx-1. We therefore believe that both GPx-1 and PHGPx are involved in the regulatory network of the 12-lipoxygenase pathway in platelets and other mammalian cells. Moreover, the diminution of hydroperoxide tone in platelets incubated with arachidonic acid leads primarily to the formation of 12-HETE, whereas the increase in hydroperoxide tone (a situation found under oxidative stress or selenium deficiency or on incubation with 12-HPETE) partly diverts the 12-lipoxygenase pathway from the reduction route to the isomerization route, thus resulting in the formation of hepoxilins.

8,11,14-Eicosatrienoic Acid↗
PubMed2004

Synthesis and characterization of AU2Se6 (A = K, Cs).

Two new ternary uranium selenides, AU(2)Se(6) (A = K, Cs), were prepared using the reactive flux method. Single crystal X-ray diffraction was performed on single crystals. The compounds crystallize in the orthorhombic Immm space group, Z = 2. CsU(2)Se(6) has cell parameters of a = 4.046(2) A, b = 5.559(3) A, and c = 24.237(12) A. KU(2)Se(6) has cell parameters of a = 4.058(3) A, b = 5.556(4) A, and c = 21.710(17) A. The compounds are isostructural to the previously reported KTh(2)Se(6). The two-dimensional layered structure is related to ZrSe(3) with the alkali metals residing in the interlayer space. The oxidation states of uranium and selenium were evaluated using X-ray photoelectron spectroscopy (XPS). Uranium was found to be tetravalent, while selenium was found to be in two oxidation states, one of which is -2. The other oxidation state is similar to that found in a polyselenide network. While this structure is known, our work examines how the structure changes through the transactinide series.

Journal Article↗
PubMed1989

Recent developments in trace element metabolism and function: newer roles of selenium in nutrition.

Until recently, studies of the function of selenium focused on the selenoenzyme, glutathione peroxidase. However, the recognition that several metabolic effects of selenium are not associated with glutathione peroxidase has forced a re-evaluation of the function of this enzyme and the element. Hepatic glutathione peroxidase contains a significant percentage of the regulated selenium in the rat and is more sensitive to selenium deficiency than other selenoproteins. Thus, in addition to its enzymatic activity, it might have a storage function for the element. Another selenoprotein, designated selenoprotein P, has been found in rat plasma and has been quantitated. Its function is not yet known, but it has been postulated to be a transport protein for selenium and a defense against oxidant stress. Understanding the nutritional effects of selenium will require better characterization of glutathione peroxidase, selenoprotein P and other selenoproteins.

Animals↗
PubMed1997

[Relationships between selenium deficiency and 3,5,3'-triiodothyronine (T3) synthesis].

Several enzymes, the main being type I 5' deiodinase, ensure thyroxin (T4) into 3,5,3'-triiodothyronine (T3) deiodination, both in the thyroid and in peripheral tissues. One of the feature of this enzymatic reaction is its regulation. It depends in part on individual selenium and iodine status. It has been shown by an analysis of thyroid hormones concentrations variations, when one of these trace elements is missing. During thyroid hormone synthesis, selenium and iodine are also implied in oxidative process control. Then, how selenium and iodine status balance modifications contribute to thyroidal diseases outbreak, becomes easier to understand. Besides, providing, adapted to individual requirements, selenium and iodine supplies could be useful for hypothyroidism and hyperthyroidism treatment.

Animals↗
PubMed2005

Studies of selenium in environmental samples and synthetic mixtures by spectrophotometry.

A rapid, highly sensitive and selective spectrophotometric method for the determination of traces of selenium(IV) is described. The method is based on oxidation of p-nitroaniline by selenium(IV) followed by coupling reaction with N-(1-naphthalene-1-yl)ethane-1,2-diamine dihydrochloride (NEDA) in neutral medium to give red colored derivative with lambda(max) 515 nm and is stable for more than 10 days at 35 degrees C. Beer's law is obeyed for selenium(IV) in the concentration range of 0.02-3.2 microg ml(-1) at the wavelength of maximum absorption. The optimum reaction conditions and other analytical parameters were investigated to enhance the sensitivity of the present method. The detailed study of various interferences made the method more selective. The proposed method was successfully applied to the analysis of selenium in polluted water, natural water samples, plant material, soil samples, and synthetic mixtures. The results obtained were agreed with the reported methods at the 95% confidence level. The performance of proposed method was evaluated in terms of Student's t-test and Variance ratio f-test which indicates the significance of proposed method over reported method.

Aniline Compounds↗
PubMed1994

Effect of alcohol consumption on blood antioxidant nutrients and oxidative stress indicators.

The effects of alcohol consumption on plasma concentrations of antioxidant vitamins (alpha-tocopherol and ascorbic acid), selenium, and markers of oxidative stress, especially malondialdehyde (MDA) and autoantibodies directed to MDA adducts to proteins (Ig-NH2-MDA) were investigated in a large population of 417 supposedly healthy men who consumed only low or moderate amounts of alcohol as compared with 102 alcoholic patients without severe liver disease, who were studied both before and after 21 d of withdrawal treatment. Plasma concentrations of alpha-tocopherol, ascorbic acid, and selenium were lower in alcoholics than in men who drank low amounts of alcohol (P < or = 0.001), whereas MDA and Ig-NH2-MDA were higher (P < or = 0.001). Plasma concentrations of alpha-tocopherol and selenium remained unchanged after the withdrawal period, whereas ascorbic acid (P < or = 0.01), MDA, and Ig-NH2-MDA concentrations decreased (P < or = 0.001). Adjustment of data for circulating lipids and nutritional intake suggests a specific effect of alcohol on antioxidant vitamins, independent of nutritional status.

Adult↗
PubMed2006

Selenium and sulforaphane modify the expression of selenoenzymes in the human endothelial cell line EAhy926 and protect cells from oxidative damage.

OBJECTIVE: We examined the ability of sulforaphane and selenium to modify the expression of thioredoxin reductase (TR-1) and the glutathione peroxidases (GPX-1 and GPX-4) in EAhy926 cells. The effectiveness of these agents to protect cells against peroxidative damage was also assessed. METHODS: EAhy926 cells were supplemented with 40 nM of selenite and/or sulforaphane (10 microM) for 72 h and the expression of TR-1, GPX-1, and GPX-4 was assessed. Parallel cultures of selenium- and sulforaphane-treated cells were exposed to tertiary butyl hydroperoxide (t-BuOOH; 0-500 microM) for 20 h, and cell integrity was determined by the percentage of lactate dehydrogenase retained by the cellular layer. RESULTS: Selenite treatment increased the concentration of TR-1 (1.6 +/- 0.17 fold, P < 0.05), GPX-1 activity (8.2 +/- 1.08 fold, P < 0.001), and GPX-4 activity (3.1 +/- 0.25 fold, P < 0.001). Sulforaphane induced TR-1 expression in selenium-deficient cells (1.83 +/- 0.11 fold, P < 0.001) and selenium-supplemented cells (2.90 +/- 0.17 fold, P < 0.001) but had no inductive effect on GPX-1 or GPX-4. The combination of selenite and sulforaphane produced an increase in TR-1 expression that was significantly greater (P < 0.001) than that achieved when each agent was added alone. Selenium and sulforaphane acted in a synergistic manner to protect cells from damage caused by t-BuOOH. The susceptibility of cells to damage by t-BuOOH increased in this order: control > sulforaphane > selenite > selenite + sulforaphane (P < 0.0001). CONCLUSION: In endothelial cells, sulforaphane increases TR-1 but not GPX-1 and GPX-4 and in doing so confers protection against oxidative damage induced by lipid hydroperoxides. The results highlight the potential important role of TR-1 over the GPXs in protecting endothelial cells from oxidative cell damage. We also suggest that our results indicate a potential beneficial role for sulforaphane in protecting the vascular endothelium from oxidative damage.

Anticarcinogenic Agents↗
PubMed1993

Selenium status and lipoproteins in healthy and diabetic children.

Selenium and the selenium-dependent glutathione peroxidase (GSH-Px) were measured in healthy and diabetic children from Germany and Hungary. Hyperglycemia and hyperlipidemia are present in diabetes mellitus and they are associated with increased lipid peroxidation. The selenium content of erythrocytes, whole blood and plasma, as well as of plasma glutathione peroxidase activity, were found to be low in the healthy Hungarian children compared to the healthy Germans. Both groups of diabetics had significantly higher blood selenium (1.05 +/- 0.14 versus 0.86 +/- 0.1 mumol/L in Hungarians, 1.34 +/- 0.21 versus 1.12 +/- 0.22 mumol/L in Germans) and higher plasma selenium (0.89 +/- 0.15 versus 0.68 +/- 0.01 mumol/L in Hungarians and 1.01 +/- 0.2 versus 0.88 +/- 0.19 mumol/L in Germans) than the healthy children of the same countries. In all diabetic children the plasma glutathione peroxidase activity and triglycerides were higher and the plasma HDL-cholesterols (HDLC = high density lipoprotein-cholesterol) lower than those in healthy controls. The patients showed linear correlations between blood glucose and plasma glutathione peroxidase activity, as well as in erythrocyte glutathione peroxidase activity with triglycerides (TG) and an inverse correlation with HDL-cholesterol. Plasma selenium correlated only in healthy children with triglycerides, cholesterol and HDL-cholesterol. Irrespective of the geographical region diabetics had a higher selenium status than healthy children. In addition, we found correlations between selenium and lipoproteins in the reference group. The mode of glycation, oxidative procedures and the selenium binding to lipoproteins could explain the different associations in the healthy and diabetic children.

Adolescent↗
PubMed1997

Measuring the oxidation of heme compounds in heart homogenates from rats supplemented with dietary antioxidants.

Protection by antioxidant nutrients against oxidative damage in rat heart homogenates was studied. Following spontaneous oxidation of heart homogenates from rats fed vitamin E, selenium, or beta-carotene, oxidized heme proteins (OHP) and thiobarbituric acid reactive substances (TBARS) were measured. The absorbance spectra of oxidized and reduced heme proteins were analyzed with a heme spectral analysis program (HSAP) developed in this laboratory. HSAP is a multicomponent analysis program that uses successive approximations and computer spread-sheet solver functions to deconvolute a complex absorbance spectrum into individual heme protein spectra. Vitamin E markedly decreased formation of OHP, and vitamin E, selenium, or beta-carotene significantly lowered the production of TBARS during spontaneous oxidation of heart homogenates compared with homogenates from rats fed antioxidant-deficient diets. Pyridine hemochrome analysis showed that the total amounts of heme proteins present in the homogenates decreased during the oxidative incubation period. The formation of OHP correlated significantly with the amount of TBARS produced and could be simulated as a function of the oxidative and protective reactions involved in the oxidation of rat heart homogenates.

Animals↗
PubMed2003

Specific spectrophotometric method with trifluoroacetic acid for the determination of selenium(IV) in selenitetriglycerides.

The role of selenium as an antioxidant and anticancer agent is very well documented in the literature. Selenium compound showing the highest activity as a free radicals scavenger and as an anticancer agent should contain selenium at +4 oxidation level. The synthesis of selenitetriglycerides (named selol) was carried out in the Department of Drug Analysis at Warsaw Medical University (Polish Patent 1999). Selenitetriglycerides showed a dimeric structure. In a single dose toxicity studies performed in rats, LD50 was 100 mg Se kg(-1) after oral administration of selol. The subcutaneous and intraperitoneal administration of selol showed extremely low toxicity. The aim of this work was to develop a new specific method for the determination of Se(IV) in selol. We stated that selenitetriglycerides react quantitatively with trifluoroacetic acid (TFA) in dichloromethane giving a red-coloured conjugate. However, recorded spectrum showed the maximum absorption in the wavelength 380 nm. The optimal conditions of the reaction were established, namely temperature 35 degrees C and reaction time 35 min. The reaction was proved to be specific because neither selenites nor other selol constituents react with TFA. The constructed calibration curve obeyed the Lambert-Beer law in the range of 0.1-7.4 mg ml(-1). Molar absorption coefficient is epsilon =9.46 x 10(3) l mol(-1) cm(-1) and epsilon =2.36 x 10(5) l mol(-1) cm(-1) calculated for selenium and selenitetriglyceride dimer (m.w. 1972.72), respectively. Obtained results for selenium determination were confirmed by AAS method. The developed method showed specificity and high sensitivity.

Selenium↗
PubMed2003

Anti-oxidant ebselen delays microvascular thrombus formation in the rat cremaster muscle by inhibiting platelet P-selectin expression.

Ebselen, a seleno-organic compound showing glutathione per-oxidase-like activity, has potent anti-inflammatory and anti-oxidant effects. Since selenium deficiency is thought to be associated with an increased incidence of vascular thrombosis, we studied the effect of ebselen on blood cell aggregate formation and vessel occlusion in vivo. In individual microvessels of rat cremaster muscle preparations, photochemically induced thrombus formation was analyzed in detail using intravital fluorescence microscopy. In ebselen-pretreated animals (30 mg/kg ip), venular thrombus formation was significantly delayed (50% vessel occlusion: 535+/-34 s; initial stasis: 872+/-82 s; complete occlusion: 908+/-87 s) as compared to vehicle-treated controls (416+/-42; 612+/-49; 647+/-51). Moreover, ebselen significantly prolonged the kinetics of arteriolar thrombus formation and even completely prevented blood cell aggregate and thrombus formation in 88.9% of all arterioles studied (p<0.05 vs controls: 37.5%). Anti-thrombotic properties of ebselen could also be observed in a model of ferric chloride-induced microvascular thrombosis, with a low dose (5 mg/kg ip) being as effective as a high dose pretreatment (30 mg/kg ip). As assessed by flow cytometry of platelet P-selectin immunfluorescence, whole blood isolated from ebselen-treated animals revealed a significantly lower fraction of P-selectin expressing platelets when compared with that of DMSO-treated controls. In addition, oxidant stress-induced upregulation of P-selectin on isolated platelets was found dose-dependently inhibited by increasing concentrations of ebselen (10-100 micro M). Moreover, ebselen dose-dependently inhibited H(2)O(2)-induced platelet-leukocyte aggregate formation in whole blood in vitro, suggesting that the anti-thrombotic effect of ebselen is achieved by attenuation of P-selectin dependent platelet-leukocyte aggregation. Thus, ebselen represents preventive and therapeutic value for disorders with increased risk for oxidant stress-associated thrombotic events.

Animals↗