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PubMed1997

Combined effects of lipid peroxidation and antioxidant status on carotid atherosclerosis in a population aged 59-71 y: The EVA Study. Etude sur le Vieillisement Artériel.

There are few epidemiologic studies of the effects of lipid peroxidation and antioxidant status on atherosclerosis. The relation of lipid peroxidation evaluated by thiobarbituric acid-reactive substances (TBARS) and biological markers of antioxidant status to ultrasonographically assessed carotid atherosclerosis was examined from baseline data of a longitudinal study on cognitive and vascular aging (Etude sur le Vieillisement Artériel, the EVA Study). The study sample was composed of 1187 mean and women aged 59-71 y without any history of coronary artery disease or stroke. Ultrasound examination included measurements of intima-media thickness (IMT) on the common carotid arteries (CCAs) and at the site of plaques. After adjustment for conventional cardiovascular risk factors, erythrocyte vitamin E was significantly and negatively associated with CCA-IMT in both men and women whereas plasma selenium and carotenoids were not. No association was found between TBARS and CCA-IMT in either sex. However, TBARS were significantly higher in men with carotid plaques than in those without. This association was strengthened in men with concentrations of erythrocyte vitamin E, plasma selenium, and carotenoids below the lowest quartile. Our findings give some epidemiologic support to the hypothesis that lipid peroxidation and low antioxidant status are involved in the early phases of atherosclerosis.

Aged↗
PubMedDate not supplied

Effects of metallic antioxidants on cadmium-catalyzed peroxidation of arachidonic acid.

In the present study, the reaction mixtures (cadmium chloride with arachidonic acid) were preincubated at 37 degrees C for 24 h prior to the measurement of malondialdehyde (MDA) by high performance liquid chromatography (HPLC). The cadmium-catalyzed reactions were also compared to those in the presence of selenium (Se), zinc (Zn) or germanium (Ge), metallic antioxidants. Our results showed that the toxic effects of cadmium cause lipid peroxidation of arachidonic acid by the catalytic process. The addition of metallic antioxidants to the reaction mixtures, might be useful in protecting against Cd-induced lipid peroxidation.

Antioxidants↗
PubMed2003

The effect of selenium on immune functions of J774.1 cells.

The J774.1 macrophage cell line was used as a tool to investigate the influence of selenium on macrophage function. In vitro selenium supplementation enhanced phagocytosis, degranulation by the release of beta-glucuronidase after N-formyl-methionyl-leucyl-phenylalanine (FMLP) or cytochalasin B, and the production of superoxide anion after phorbol myristate acetate stimulation of these cells, while the release of nitric oxide was not affected by the selenium status. Selenium supplementation enhanced significantly (p < 0.05) the release of tumor necrosis factor (5-fold), interleukin-1 (3-fold) and interleukin-6 (2.5-fold) after 10 microg/ml lipopolysaccharide stimulation compared to selenium-deficient cells.

Animals↗
PubMed1995

Bioremediation of organic and metal contaminants with dissimilatory metal reduction.

Dissimilatory metal reduction has the potential to be a helpful mechanism for both intrinsic and engineered bioremediation of contaminated environments. Dissimilatory Fe(III) reduction is an important intrinsic process for removing organic contaminants from aquifers contaminated with petroleum or landfill leachate. Stimulation of microbial Fe(III) reduction can enhance the degradation of organic contaminants in ground water. Dissimilatory reduction of uranium, selenium, chromium, technetium, and possibly other metals, can convert soluble metal species to insoluble forms that can readily be removed from contaminated waters or waste streams. Reduction of mercury can volatilize mercury from waters and soils. Despite its potential, there has as yet been limited applied research into the use of dissimilatory metal reduction as a bioremediation tool.

Bacteria↗
PubMed2001

Selenium: a key element that controls NF-kappa B activation and I kappa B alpha half life.

Treatment of mammalian cells with hydrogen peroxide induces the nuclear translocation of the transcription factor NF-kappa B and its binding to kappa B DNA sequences present in the promoter region of numerous genes. The role of selenium in NF-kappa B activation was analyzed in human T47D cells overexpressing the seleno-dependent detoxifiant enzyme glutathione peroxidase. Following exposure to H(2)O(2), these cells showed a seleno-dependent decreased accumulation of intracellular ROS and NF-kappa B activation. This phenomenon was correlated with an inhibition of the nuclear translocation of NF-kappa B (p50 subunit) and with an absence of I kappa B alpha degradation. We also report that the half-life of I kappa B alpha in untreated cells was increased two-fold by the overexpression of active glutathione peroxidase. These results suggest that selenium is a key element that through its modulation of glutathione peroxidase activity can inhibit NF-kappa B activation and can up-regulate I kappa B alpha normal half life.

Animals↗
PubMedDate not supplied

Effect of experimental oxidative stress on steroidogenesis and DNA damage in mouse testis.

The objective of the present study was to evaluate the effect of oxidative stress induced by feeding various levels of selenium on steroidogenesis and DNA damage in mouse testes. To create various levels of oxidative stress in mice, diets with three different Se levels were fed to separate groups for 8 weeks. Group 1 animals were fed a yeast-based diet, which was considered a Se-deficient diet (0.02 ppm). Group 2 and 3 animals were fed a Se-deficient diet supplemented with 0.2 and 1 ppm Se as sodium selenite, respectively. After completion of the diet feeding, estimations were carried out, and results were compared with those of group 2. A significant decrease in Se levels was observed in group 1 animals, whereas they were greatly enhanced in group 3. Glutathione peroxidase (GSH-Px) activity was greatly reduced in both the liver and testes in group 1, whereas no significant changes were found in GSH-Px activity in group 3. Serum luteinizing hormone, follicle-stimulating hormone (FSH), and testosterone levels were reduced in group 1. Significant decreases of sperm number and motility were observed in group 1 when compared to group 2 male mice. No changes in these parameters were observed in group 3. DNA fragmentation was observed in both groups 1 and 3; however, the damage was more prevalent in group 1. The results clearly demonstrate the effect of oxidative stress generated by feeding various Se levels on the steroidogenesis and DNA fragmentation in mice testes.

Animals↗
PubMed1982

Dry ashing, hydride generation atomic absorption spectrometric determination of arsenic and selenium in foods.

A dry ashing, flameless atomic absorption spectrometric method was evaluated to determine arsenic and selenium in foods. Samples were dry-ashed with Mg(NO3)2-MgO and dissolved in HCl. Selenate was reduced to selenite by boiling in 4N HCl. Selenate was reduced to selenite by boiling in 4N HCl, and arsenate to arsenite by treatment with KI. Hydrides of arsenic and selenium were generated by the addition of NaBH4 and were swept by nitrogen and hydrogen into a thermally heated silicate tube furnace. The detection limit was about 5 ppb for each element based on a 10 g sample. Analytical results obtained for several samples of NBS reference materials agreed with the certified values. The procedure was evaluated by another laboratory and results were satisfactory.

Arsenic↗
PubMed1999

Selenium and host defence towards viruses.

The association between viral disease and nutrition has long been thought to be due to effects on the host immune system. This theory suggests that when a host is malnourished, the immune system is compromised, and thus increased susceptibility to viral infection will occur. However, the virus itself may also be affected by the nutritional status of the host. We have demonstrated that a normally-benign strain of coxsackievirus B3 (CVB3/0) becomes virulent in either Se-deficient or vitamin E-deficient mice. Although the deficient animals are immunosuppressed, the virus itself is also altered. Six nucleotide changes were found in the virus that replicated in the deficient mice, and once these mutations occurred, even mice with normal nutrition became susceptible to disease. Thus, the nutritional status of the host was able to transform an avirulent virus into a virulent one due to genomic changes in the virus. We believe that a common mechanism of oxidative stress is the underlying cause of the genetic changes. Both vitamin E and Se act as antioxidants, and benign virus inoculated into GSH peroxidase (EC 1.11.1.9)-knockout mice will also convert to virulence due to genomic changes. Our work points to the importance of host nutrition during a viral disease, not only from the perspective of the host, but from the perspective of the viral pathogen as well.

Animals↗
PubMed1997

Selenium and the thioredoxin redox system: effects on cell growth and death.

Thioredoxin is a redox protein found overexpressed in some human tumors. Thioredoxin is secreted by tumor cells and enhances the sensitivity of the cancer cells to other growth factors. Redox activity is essential for stimulation of cell growth by thioredoxin. Cells transfected with thioredoxin cDNA show increased tumor growth and decreased apoptosis in vivo and decreased sensitivity to apoptosis induced by a variety of agents both in vitro and in vivo. Cells transfected with a redox-inactive mutant thioredoxin show inhibited tumor growth in vivo. Dietary selenium has been shown to prevent some forms of human cancer. Selenocysteine is an essential component of thioredoxin reductase, the flavoenzyme that is responsible for the reduction of thioredoxin. Selenium added to the culture medium increases thioredoxin reductase activity due to an increase in thioredoxin reductase protein but mostly due to an increase in the specific activity of the enzyme. Some diaryl chalcogenide (selenium and tellurium) compounds have been studied as inhibitors of thioredoxin reductase. The most active were diaryl tellurium compounds, which were noncompetitive inhibitors of thioredoxin reductase with Ki values of 2-10 microM. Several of the compounds inhibited cancer cell colony formation in vitro with IC50s as low as 2 microM.

Apoptosis↗
PubMed1995

Physiological mechanisms regulating the conversion of selenite to elemental selenium by Bacillus subtilis.

We have demonstrated that the common soil bacterium, Bacillus subtilis, reduces selenite to an insoluble and much less toxic product--the red form of elemental selenium. Reduction was effected by an inducible system that appears to deposit elemental selenium between the cell wall and the plasma membrane. Glucose and sucrose supported selenite reduction. Although malate and citrate supported growth, no significant reduction of selenite occurred, indicating the importance of the redox state of the culture substrate. Selenite reduction in the millimolar concentration range (i.e., cultures supplemented with 1 mM selenite) was not affected by a ten-fold excess of nitrate or sulfate--compounds that serve as alternate electron acceptors and antagonize selenite reduction by anaerobic bacteria. Similarly, nitrite and sulfite did not significantly affect the rate or extent of selenite reduction. B.subtilis was able to grow and produce selenium (Se degree) at selenite concentrations ranging from 0.6 microM to 5 mM (50 ppb to 395 ppm selenium). At the lowest selenite concentration tested, 50 ppb selenium, B.subtilis removed 95% of the selenite from the liquid phase. The results suggest that selenite is reduced via an inducible detoxification system rather than dissimilatory electron transport. The findings establish the potential utility of B.subtilis for the bioremediation of selenite-polluted sites.

Bacillus subtilis↗
PubMed2000

The importance of selenium to human health.

The essential trace mineral, selenium, is of fundamental importance to human health. As a constituent of selenoproteins, selenium has structural and enzymic roles, in the latter context being best-known as an antioxidant and catalyst for the production of active thyroid hormone. Selenium is needed for the proper functioning of the immune system, and appears to be a key nutrient in counteracting the development of virulence and inhibiting HIV progression to AIDS. It is required for sperm motility and may reduce the risk of miscarriage. Deficiency has been linked to adverse mood states. Findings have been equivocal in linking selenium to cardiovascular disease risk although other conditions involving oxidative stress and inflammation have shown benefits of a higher selenium status. An elevated selenium intake may be associated with reduced cancer risk. Large clinical trials are now planned to confirm or refute this hypothesis. In the context of these health effects, low or diminishing selenium status in some parts of the world, notably in some European countries, is giving cause for concern.

Acquired Immunodeficiency Syndrome↗
PubMed1999

The selenium link: the missing link in our understanding of biochemical trigger reactions?

'Inorganic' selenium (Se), e.g. selenite and selenate, is assumed to be transformed into selenide and to be incorporated into selenoproteins, but this has never been proved. There is evidence, however, that vitamin C reduces selenite to elemental Se. Elemental sulphur (S) and Se bind easily to sulphides and selenides, forming links containing two or more S or Se atoms. Such links exist in natural minerals and have been found in proteins in living organisms. There are many indications that selenocysteine in special proteins combines with elemental Se to form Se links that transfer electrons from redoxable agents to oxygen (O2). This implies a reduction to hydrogen peroxide (H2O2) or H2O, while gaining energy and achieving trigger effects. H2O2 supplies anaerobic reactions with energy eventually via adenosine 5'-triphosphate (ATP) or guanosine 5'-triphosphate (GTP). Without Se links, redoxable agents can be oxidized by oxygen, which leads to the formation of oxygen products and inhibition of further electron transference. Nitrous oxide (NO) is one product of oxidation that, firmly binding to heme structures, may result in a system of protection. NO can prevent O2 from binding to them and thereby stop destroying oxidations.

Animals↗
PubMed1996

Maternal selenium levels and sudden infant death syndrome (SIDS).

BACKGROUND: The possibility is tested that low anti-oxidant status and/or low levels of selenium (Se) might predispose to Sudden Infant Death Syndrome (SIDS). AIM: This study was undertaken to collect evidence on the Se status of pregnant and non-pregnant women and newborn babies and to establish whether babies who later died of cot death had significantly divergent levels of blood Se at birth. METHODOLOGY: Aliquots of blood were collected from all newly pregnant mothers in Tasmania and from the cords of all newborn babies. These were analysed for Se and glutathione peroxidase (GPx) content and compared by season and with non-pregnant, age standardised blood donors in three areas of Tasmania and three mainland Australian States. RESULTS: Cot death babies' cordbloods were not significantly different in Se or GPx-status, in this small sample, from those of other babies, nor was a seasonal variation in these parameters demonstrated among 390 randomly selected Tasmanian mothers. Mothers-to-be showed a decrease in enzyme levels during pregnancy and Tasmanian blood donors had significantly lower levels than donors from other States. CONCLUSION: While no evidence can safely be drawn about a relationship between Se or GPx-status and SIDS, this study provides base level measures for populations showing that Tasmanian residents have low levels of these anti-oxidants.

Adult↗
PubMed2004

Comparison of chemopreventive effects of Vitamin E plus selenium versus melatonin in 7,12-dimethylbenz(a)anthracene-induced mouse brain damage.

In this work, the protective effect of Vitamin E plus selenium (Vit E+Se) and melatonin against 7,12-dimethylbenz(a)anthracene (7,12-DMBA)-induced changes in superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT) and carbonic anhydrase (CA) activities and malonedialdehyde (MDA) levels of mouse brain were compared. 12-month old mice were divided into four groups each including 10 animals. The first group served as control group. The second group was treated with 7,12-DMBA (20 mg/(kg day)). The third group was treated with 7,12-DMBA and Vitamin E (90 microg/(individual day)) and selenium (1.8 microg/(individual day)) simultaneously. The fourth group was treated with 7,12-DMBA and melatonin (4.2 mg/(kg day)) simultaneously. Treatment continued for 21 days after which the mice were sacrificed and brain homogenates were prepared. 7,12-DMBA treated group exhibited significantly decreased levels of brain SOD, GSHPx, CAT and CA activities and increased MDA levels as compared to control. Vitamin E+Se fully or partially restored enzyme inhibition except for SOD. Lipid peroxidation was also reduced in Vitamin E+Se treated group. Melatonin provided a better protection for SOD, GSHPx and CAT, and a plausible protection for CA activity. Protection against lipid peroxidation measured as MDA in melatonin treated group was appreciable although slightly lesser than the protection provided by Vitamin E+Se. The results imply that Vitamin E+Se and melatonin both provide chemoprevention against 7,12-DMBA-induced oxidative stress in mouse brain.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Redox modulation of selenium binding proteins by cadmium exposures in mice.

The mechanism of the antagonistic behaviour of selenium (Se) against cadmium (Cd) toxicity is investigated. This study reports the distribution of Cd at the organ and subcellular level after chronic treatments. The possible role of the selenium binding proteins (SBP) during Cd exposure are also evaluated. Kidney concentrates more Cd than liver following 8 weeks of treatment. Simultaneous administration of Se reduced Cd accumulation in Kidney. This affect did not occur in liver. Among the subcellular fractions, the maximum concentrations of both of the elements were found in the cytosol. The overall uptake of 75Se was enhanced in the cytosol of kidney and liver of the Cd treated animals. These observations support a hypothesis that selenium is complexed with cadmium. The increase in the labeling of SBP as a result of Cd exposures may reflect a change in the conformation of the protein molecule. These proteins (SBP) contain a sequence motif, which may be an active redox centre. Also, Cd significantly reduced the glutathione level, thereby disrupting the thiol/disulfide balance. This in turn may affect the redox status of the proteins leading to a 75Se or 75Se-Cd complex with SBP.

Animals↗
PubMed2003

Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency.

The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors, including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally induced inflammatory heart disease.

Animals↗
PubMed1999

Lipid peroxidation and antioxidant system in the blood of cancerous patients with metastasis.

Free-radical-mediated damages may play an important role during metastasis. To investigate their relevance in the metastatic process MDA levels, glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities, and selenium, zinc and copper contents were determined in plasma and erythrocytes from 20 cancerous patients with metastasis and 30 age-matched controls. Significantly higher concentrations of MDA in plasma as well as in erythrocytes were found comparing to the control group. In both plasma and erythrocytes, GPX activity and selenium and zinc levels were significantly lower in patients than in controls. However, SOD activity in erythrocytes and copper levels in both plasma and erythrocytes were significantly higher in patients. The impaired antioxidant system may favor accumulation of free radicals which may induce the process of metastasis. On the other hand, it is possible that the antioxidant system is impaired as a consequence of abnormality in the antioxidative metabolisms due to the cancer process.

Adult↗