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PubMed1971

The effect of vitamin E on the intracellular distribution of the different oxidation states of selenium in rat liver.

1. The liver intracellular distribution of (75)Se, (75)Se(2-) and (75)SeO(3) (2-) formed from orally administered Na(2) (75)SeO(3) was studied in rats given four different dietary treatments. 2. Subcellular fractionation was done by using sucrose density gradients in a B XIV zonal centrifuge rotor, and conditions were established so that separation of lysosomal, mitochondrial, smooth- and rough-surfaced endoplasmic reticulum, and soluble fractions was achieved. 3. Marker enzymes acid phosphatase, succinate-2 - p - iodophenyl - 3 - p -nitrophenyl - 5 - phenyltetrazolium reductase and glucose 6-phosphatase were used, together with electron microscopy, to establish the identity of the fractions. 4. The dietary treatments investigated were: (a) vitamin E-deficient diet for 3 months, re-fed with vitamin E during the terminal 5 days; (b) vitamin E-deficient diet; (c) adequate diet; (d) vitamin E- and selenium-deficient diet, re-fed with vitamin E during the terminal 5 days. 5. In adequately fed rats, selenide was particularly associated with the mitochondrial fractions; in vitamin E-deficient rats, little selenide was found and the buoyant density of the mitochondria was increased, whereas re-feeding with vitamin E showed a restoration of the normal pattern. In vitamin E- and selenium-deficient rats, re-fed with vitamin E, there was no tendency for selenide to be localized in the mitochondria. 6. In the microsomal regions of the gradients, adequately fed rats showed a concentration of selenide, particularly in the smooth endoplasmic reticulum fractions, and to a lesser extent in the rough endoplasmic reticulum fractions. This was not observed in vitamin E-deficient rats, and the normal pattern was restored on re-feeding with vitamin E, both in rats given the vitamin E-deficient diet and the vitamin E- and selenium-deficient diet. 7. Some selenide was also found in the soluble fractions, when vitamin E was present, and a substantial proportion of this selenide was found to pass through a dialysis membrane. 8. These results are taken to support our hypothesis that the active form of selenium may be selenide located in non-haem iron-containing proteins, and that the function of vitamin E may be to protect the selenide from oxidation.

Animals↗
PubMed1998

Selenium deficiency in tissue culture: implications for oxidative metabolism.

BACKGROUND: Selenium is located at the catalytic site of the enzyme glutathione peroxidase, and with selenium deficiency the activity of glutathione peroxidase is decreased. Cell culture is an important tool for studying oxidative processes-that is generation and metabolism of oxygen-derived metabolites in the gastrointestinal system. Cell culture is also used to understand the mechanisms of cell injury by oxygen-derived metabolites. METHODS: To assess the importance of the selenium content of cell culture media, Caco-2 cells and the hepatoma-derived cell lines, Hep3B and HepG2, were grown to confluence and placed in media with various concentrations of selenium. After 7 to 14 days, cells were harvested and assayed for glutathione peroxidase, lactate dehydrogenase, and protein content. RESULTS: Cells maintained in media unsupplemented with selenium demonstrated a progressive decrease in glutathione peroxidase activity. Cells maintained in media supplemented with various concentrations of selenium demonstrated a dose-dependent increase in glutathione peroxidase until a plateau was reached. The plateau was reached at approximately 400 times the selenium concentration routinely used in cell culture. In the Caco-2 and hepatoma cells, no toxicity was observed at selenium supplementation five times the lowest concentration needed to reach a plateau. CONCLUSIONS: Cell culture media are routinely deficient in selenium, and cells that are cultured in this medium are deficient in glutathione peroxidase activity. Studies of oxidative metabolism based on cultures deficient in selenium may yield results that could be falsely interpreted. The addition of 1 nM selenium is sufficient for these cell lines to reach a plateau for intracellular glutathione peroxidase activity. These observations may have important ramifications for the study of reactive oxygen metabolite injury in cell culture.

Caco-2 Cells↗
PubMed1989

Oxidative damage in selenium deficient hearts on perfusion with adriamycin: protective role of glutathione peroxidase system.

The protective effects of the glutathione peroxidase system against functional damage induced by perfusion of isolated hearts with adriamycin, an anthracycline antibiotic, were studied. We used selenium deficient rats, in which cardiac glutathione peroxidase activity was only 3% of control rats. Both contractile tension and coronary flow decreased during perfusion with the antibiotic. The degree of decline was significantly greater in the selenium deficient hearts than in the control hearts. The increase in malondialdehyde, a product of lipid peroxidation, induced by adriamycin perfusion was more evident in selenium deficient hearts, though the level of reduced glutathione was well maintained. Isolated mitochondrial function also decreased after aerobic adriamycin perfusion and the decrease was greater in selenium deficient rats. These observations indirectly suggest that the decrease in cardiac function induced by adriamycin is protected by the glutathione peroxidase system and that the decrease may be due, at least in part, to damage to the mitochondria caused by oxygen radicals generated by adriamycin.

Animals↗
PubMed1991

[Tangier disease--a "free radical"-associated disease. Results of HDL and anti-oxidant therapy with selenium and D-alpha tocopherol].

In a 26-year-old patient there have been benign enlargements of the lymphatic nodes and a splenomegaly since the end of the adolescence. In the 21st year of age the diagnosis of a Tangier disease was made. Allogenic HDL-rich serum fraction (COHN IV/1-fraction, prepared according to the modified method 6) infused under therapeutic aspect led to a prolonged increase of the serum total cholesterol and of the thrombocytes. The results pled for an activation of the reverse cholesterol transport. Excessively high malonic dialdehyde concentrations in the serum were relating to a "free radical"-associated metabolic defect, which was caused by the hypocholesterolaemia, the reduced transport capacity of vitamin E in the plasma and the nutrition poor in selenium and cholesterol, respectively. Under a nutritive antioxidant supplementation with sodium selenite and D-alpha-tocopherol a slight increase of the total cholesterol, of the thrombocytes as well as a normalization of the MDA values could be reached. The chronic oxidative stress appeared in the patient in a distinct lipofuscinosis of the skin and formations of naevus-cell naevi as an expression of massive denaturations of protein-lipids. In the Tangier disease we must reckon with an increased mutagenic effect of free radicals with an additional DNS repair capacity as well as an increased sensitivity to radical-generating cancerogenic xenobiotics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Impacts of glutathione peroxidase-1 knockout on the protection by injected selenium against the pro-oxidant-induced liver aponecrosis and signaling in selenium-deficient mice.

Previous research has suggested that repletion of cellular glutathione peroxidase (GPX1) activity by a single injection of Se was dissociated from the Se protection against the pro-oxidant-induced liver necrosis in Se-deficient rodents. Using the GPX1 knockout (GPX1-/-) mice, TUNEL assay, and apoptosis gene expression microarray, we have demonstrated strikingly different impacts of GPX1 knockout on hepatotoxicity and the related signaling induced by an intraperitoneal injection of 12.5 mg paraquat/kg body weight (b.wt.). In both Se-deficient GPX1-/- and wild-type (WT) mice, the paraquat did not induce typical liver necrosis, rather aponecrosis or necrapoptosis, a syncretic process of cell death sharing characteristics of both apoptosis and necrosis. The severity of liver aponecrosis and the associated mortality were reduced to a much greater extent by an injection of Se (ip, 50 microg/kg b.wt. as Na2SeO3) prior to paraquat stress in the WT mice, compared with the GPX1-/- mice. The induced liver aponecrosis seemed to be more apoptotic in the GPX1-/- mice but more necrotic in the WT mice. The paraquat-mediated gene or protein expression of proapoptotic Bax, Bcl-w, and Bcl-X(S), cell survival/death factors GADD45, MDM2, c-Myc, and caspase-3 was upregulated, but that of antiapoptotic Bcl-2 was downregulated in the GPX1-/- mice vs. the WT mice. Overall, these differences between the two groups of mice were related to a low level of liver GPX1 activity in the WT mice that represented < 4% of the normal physiological level. Therefore, the low level of GPX1 activity in the Se-deficient mice can exert a potent role in defending against liver aponecrosis induced by moderate oxidative stress.

Analysis of Variance↗
PubMed1994

Liver microsome and flavin-containing monooxygenase catalyzed oxidation of organic selenium compounds.

Eight commercially available selenides, a selenol, and selenourea were examined for substrate activity with purified pig liver flavin-containing monooxygenase (FMO). While none of the aromatic heterocyclic selenides tested showed detectable activity, all dialkyl- and alkylaryl-selenides free from ionic groups stimulated NADPH- and FMO-dependent oxygen uptake. With limiting substrate the molar ratio of oxygen reduced to selenide added was 1:1. Analysis of products from N-[2-(methylseleno)ethyl]benzamide demonstrated that the selenide was quantitatively oxidized to selenoxide. Further oxidation of either the FMO-generated or synthetic selenoxides was not detected. The dialkyl- and alkylaryl-selenoxides are potent thiol oxidants and reaction rates for the oxidation of thiols by methylphenylselenoxide and N-[2-(methylseleninyl)ethyl]benzamide followed second order kinetics with rate constants from 3-4 x 10(3) M-1 s-1 at pH 7.4, 37 degrees C. The rapid oxidation of thiols by these selenoxides demonstrates that the oxidation of selenides to selenoxides catalyzed by crude tissue preparations can be measured by following selenide-dependent oxidation of thiocholine by the procedure described earlier for the oxidation of thiourea (WXA Guo and D. M. Ziegler, 1991, Anal. Biochem. 198, 143-148). Activity measurements by this procedure indicated that the oxidation of dialkyl selenides by rat, guinea pig, or pig liver microsomes was catalyzed primarily by a monooxygenase with the properties of FMO. However, from 20 to 40% of the microsome-catalyzed oxidation of selenides bearing aryl substituents was sensitive to N-benzylimidazole, suggesting that P450-dependent monooxygenases also contribute, at least in part, to the oxidation of these xenobiotics.

Animals↗
PubMed1996

Determination of different oxidation states of arsenic and selenium by inductively coupled plasma-atomic emission spectrometry with ion chromatography.

Recent regulation in Japan requires more sensitive trace analysis methods for the determination of arsenic and selenium and their oxidation states As(III) and (V), Se(IV) and (VI). The hydride generation (HG) technique is usually used in combination with AAS and ICP-AES to increase sensitivity. However, hydrochloric acid is mostly used to acidify the sample solution in HG. Isobaric interferences due to chlorine-related species cause mass spectral problems when the same solution is used for the determination of these elements by ICP-MS. In this study, different oxidation states of As and Se were determined by coupling ion chromatography (IC) to an ICP-AES instrument. An HG technique was used to introduce test samples into the ICP. Nitric acid was employed to acidify the samples for HG. The concentrations of acid and base were kept as low as possible to reduce contamination. The formation of As and Se hydrides could be achieved without HCl, if the concentrations of acid and alkaline solutions were optimized. However, HCl was necessary for additional reduction of Se(VI) to Se(IV).

Journal Article↗
PubMed1987

Rat lung glutathione release: response to oxidative stress and selenium deficiency.

We performed experiments to characterize the glutathione-dependent metabolism occurring during tert-butyl hydroperoxide infusion in isolated perfused rat lungs and to examine the effect of selenium deficiency on this metabolism. Selenium deficiency resulted in decreased lung glutathione peroxidase activity but normal glutathione reductase activity and glutathione content. Infusion of the hydroperoxide into control lungs caused a proportional increase in tissue glutathione disulfide (GSSG) concentration and release of GSSG into the perfusate up to an infusion rate of 250 nmol of tert-butyl hydroperoxide X min-1 X 100 g body wt-1. Infusion rates greater than this resulted in continued rise of tissue GSSG concentrations but GSSG release into the perfusate plateaued. Infusion of tert-butyl hydroperoxide into selenium-deficient rat lungs resulted in much lower concentrations of tissue GSSG and GSSG release into the perfusate; however, release in the selenium-deficient rat lung was also found to be saturable at infusion rates of 450 nmol of tert-butyl hydroperoxide X min-1 X 100 g of body wt-1. Selenium deficiency in the rat decreases the rate of reduction of infused tert-butyl hydroperoxide by glutathione and may predispose the lung to free radical damage.

Animals↗
PubMed2006

Simultaneous removal of SO2 and trace SeO2 from flue gas: effect of product layer on mass transfer.

Sulfur dioxide (SO2) and trace elements are all pollutants derived from coal combustion. This study relates to the simultaneous removal of sulfur and trace selenium dioxide (SeO2) by calcium oxide (CaO) adsorption in the medium temperature range, especially the mass transfer effect of sulfate product layer on trace elements. Through experiments on CaO adsorbing different concentrations of SO2 gases, conclusions can be drawn that although the product layer introduces extra mass transfer resistance into the sorbent-gas reaction process, the extent of CaO adsorption ability loss due to this factor decreases with decreasing SO2 concentration. When the gas concentration is at trace level, the loss of CaO adsorption ability can be neglected. Subsequent experiments on CaO adsorbing trace SeO2 gas suggest that the sulfate product layer, whether it is thick or thin, has no obvious effect on the CaO ability to adsorb trace SeO2 gas.

Adsorption↗
PubMed2003

Sulfur and selenium: the role of oxidation state in protein structure and function.

Sulfur and selenium occur in proteins as constituents of the amino acids cysteine, methionine, selenocysteine, and selenomethionine. Recent research underscores that these amino acids are truly exceptional. Their redox activity under physiological conditions allows an amazing variety of posttranslational protein modifications, metal free redox pathways, and unusual chalcogen redox states that increasingly attract the attention of biological chemists. Unlike any other amino acid, the "redox chameleon" cysteine can participate in several distinct redox pathways, including exchange and radical reactions, as well as atom-, electron-, and hydride-transfer reactions. It occurs in various oxidation states in the human body, each of which exhibits distinctive chemical properties (e.g. redox activity, metal binding) and biological activity. The position of selenium in the periodic table between the metals and the nonmetals makes selenoproteins ideal catalysts for many biological redox transformations. It is therefore apparent that the chalcogen amino acids cysteine, methionine, selenocysteine, and selenomethionine exhibit a unique biological chemistry that is the source of exciting research opportunities.

Cysteine↗
PubMed1985

Lung clearance, translocation, and acute toxicity of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium oxides following deposition in rat lung.

Young adult rats were exposed via inhalation or intratracheal instillation to oxides of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium. Serial necropsies were performed to assess the metal content in organs at times up to several weeks after exposure. The lung clearance varied widely for these compounds, and the times to remove 50% of the initial burden ranged from 18 min for vanadium to 400 days for beryllium. Arsenic, cadmium, lead, selenium, and vanadium were initially soluble in lung, but a small fraction (1-20%) remained there over the long term. Extrapulmonary tissues often accumulated substantial amounts of the soluble oxides, and whole-body retention was often greater for compounds that were more soluble in lung. Arsenic, selenium, and vanadium translocated to carcass and bone. Arsenic, cadmium, lead, and selenium accumulated in the liver, and the kidney retained cadmium and lead. Beryllium, cobalt and ytterbium did not deposit at any extrapulmonary site in significant amounts. In general, the aqueous solubility of these compounds was a poor predictor for behavior in vivo because of their interaction with metabolic processes. Of the metal oxides tested for acute lethality following pulmonary deposition, cadmium was most toxic, followed by selenium, vanadium, and arsenic.

Animals↗
PubMed2005

Effects of different levels of dietary supplemental selenium on performance, lipid oxidation, and color stability of broiler chicks.

This study examined the effects of supplemental dietary selenium on growth performance, lipid oxidation, and color stability of broiler chicks. Male broiler chicks (Arbor Acres, 1 d old, total 900 chicks) were randomly assigned to 6 pens containing 30 chicks each, corresponding to each of 6 dietary treatments. Six different diets were supplied to the chicks from 3 to 6 wk of age. After 42 d of feeding, all the broilers were slaughtered conventionally at a slaughtering plant. The carcasses were packed in polyethylene bags in a manner similar to that used for retail trade and stored for 12 d at 4 degrees C. Body weight and feed efficiency were not affected by dietary selenium levels, and no adverse effect on growth was observed during the experimental period. The dietary selenium and alpha-tocopherol levels did not affect surface meat color or level of metmyoglobin accumulation. Lipid stability was improved by supplementation with 100 IU of alpha-tocopherol (P < 0.05). Dietary selenium supplementation at 8 ppm in combination with 100 IU of alpha-tocopherol, however, was more effective in reducing lipid oxidation compared with 100 IU of alpha-tocopherol/kg feed only (P < 0.05). Supplementation with 100 IU of alpha-tocopherol affected cholesterol oxidation product levels on d 7 and 12, but selenium supplementation did not have an additional effect on the reduction of cholesterol oxidation products. Therefore, an increase in the dietary selenium from 1 to 8 ppm revealed only minor improvements in the oxidative stability of chicken meat during refrigerated storage.

Animals↗
PubMed1984

The effect of vitamin E or selenium on the oxidant-antioxidant balance in rats.

Vitamin E and selenium are two components which contribute to the antioxidant potential of plasma and tissues. In the present study we aimed to define the type of tissue toxicity deriving from chronic deficiency of either vitamin E or selenium and to evaluate the reliability of peripheral markers of tissue toxicity in these conditions. We studied rats fed a vitamin E or selenium-deficient diet for 3 or 7 months and a selenium-supplemented diet. The effectiveness of the dietary treatment was confirmed by measuring vitamin E and selenium in plasma. Heart and kidney malondialdehyde (MDA), a typical product of lipid peroxidation, was significantly increased after the 3-month diet in both vitamin E- and selenium-deficient rats. The iron-binding capacity of plasma, an activity ascribed to plasma transferrin, was reduced in selenium-deficient and increased in selenium-supplemented animals. In red cells globular resistance (resistance to osmotic haemolysis) was low in vitamin E- and selenium-deficient, but high in selenium-supplemented animals. Glutathione peroxidase was also increased in selenium-supplemented rats. Platelet count did not differ from controls in any of the three conditions studied. Platelet MDA formation induced by arachidonic acid was raised in both selenium-deficient and, particularly, vitamin E-deficient groups. This can be regarded as a peripheral marker of reduced antioxidant defence at tissue level.

Animals↗