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PubMed1992

The involvement of selenium in peroxisome proliferation caused by dietary administration of clofibrate to rats.

The effects of dietary treatment with clofibrate (0.5% w/w for 10 days) on the livers of selenium-deficient male rats were examined. The peroxisome proliferation (as determined by electron microscopy) in the livers of selenium-deficient animals was much less pronounced than in the case of selenium-adequate rats and no increase in peroxisomal fatty acid beta-oxidation (assayed both as antimycin-insensitive palmitoyl-CoA oxidation and lauroyl-CoA oxidase activity) was observed in the deficient animals. On the other hand, in selenium-deficient rats clofibrate caused increases in the specific activity of microsomal lauric acid omega- and omega-1-hydroxylation and an apparent change in mitochondrial size, seen as a redistribution of mitochondria from the 600 x g(av) pellet to the 10,000 x g(av) pellet, which were approximately 50% as great as the corresponding effects on control animals. Obviously, then, these three different effects of clofibrate are not strictly coupled and may involve at least partially distinct underlying mechanisms. Initial experiments demonstrated that peroxisome proliferation could be obtained by exposing primary hepatocyte cultures derived from selenium-deficient rats to clofibric acid (an in vivo hydrolysis product of clofibrate which is the proximate peroxisome proliferator), nafenopin or mono(2-ethylhexyl)phthalate. This finding suggests that selenium deficiency does not have a direct influence on the basic process(es) underlying peroxisome proliferation, but rather has indirect effects, influencing, for example, the pharmacokinetics of clofibrate and/or hormonal factors.

Animals↗
PubMed2006

Oxidative stress and septic shock: metabolic aspects of oxygen-derived free radicals generated in the liver during endotoxemia.

This review describes the role of oxidative stress caused by endotoxin challenge in sepsis or septic shock symptoms. We observed that endotoxin injection resulted in lipid peroxide formation and membrane damage (near 60-150 kDa) in the livers of experimental animals, causing decreased levels of scavengers or quenchers of free radicals. The administration of alpha-tocopherol completely prevented injury to the liver plasma membrane caused by endotoxin, and suggested that lipid peroxidation by free radicals might occur in a tissue ischemic state, probably by disseminated intravascular coagulation (DIC), in endotoxemia. In mice, depression of Ca(2+)-ATPase activity in the liver plasma membrane may contribute to the membrane damage caused by endotoxin, and the increase of [Ca(2+)](i) in the liver cytoplasm may partially explain the oxidative stress that occurs in endotoxemia. It seems that endotoxin-induced free radical formation is regulated by Ca(2+) mobilization. Moreover, we have suggested that the oxidative stress caused by endotoxin may be due, at least in part, to the changes in endogenous zinc or selenium regulation during endotoxemia. Interestingly, the extent of TNF-alpha-induced oxidative stress may be the result of a synergism between TNF-alpha and gut-derived endotoxin. It is likely that bacterial or endotoxin translocation plays a significant role in TNF-alpha-induced septic shock. On the other hand, although nitric oxide (NO) has been implicated in the pathogenesis of vascular hyporesponsiveness and hypotension in septic shock in our experimental model, it is unlikely that NO plays a significant role in liver injury caused by free radical generation in endotoxemia.

Animals↗
PubMed2002

Associations between dietary antioxidant intake and oxidative stress in HIV-seropositive and HIV-seronegative men and women.

OBJECTIVE: To describe the relationship between dietary antioxidant intake and oxidative stress in clinically stable HIV-positive and HIV-negative adults. DESIGN: A cross-sectional study. METHODS: Average total daily dietary intakes of vitamin C, beta-carotene, alpha-tocopherol, selenium, and zinc from foods and nutritional supplements were estimated in noninstitutionalized individuals using the dietary history method. Plasma malondialdehyde (MDA) concentrations were measured by high-performance-liquid-chromatography (HPLC) whereas peripheral blood mononuclear cell glutathione (PBMC GSH) concentrations were determined spectrophotometrically by an enzymatic recycling assay. Data were analyzed in multiple linear regression models to investigate these relationships. RESULTS: Regression analysis revealed an inverse relationship between selenium intake and plasma MDA in a model that included the five dietary antioxidants ( R 2 = 0.25; p < .02) and with selenium only ( R 2 = 0.19; p < .01). Both models were adjusted for gender, smoking status, and HIV seropositivity. Antioxidant intake was not associated with PBMC GSH ( R 2 = 0.12, p = .36). In univariate analyses, oxidative stress did not significantly differ between clinically stable HIV-positive and healthy HIV-negative study subjects. CONCLUSIONS: This is the first study to characterize the relationship between dietary antioxidant intake from food and supplements with oxidative stress. The results suggested dietary selenium intake was strongly and inversely associated with plasma MDA, but dietary antioxidant intakes were not related to PBMC GSH. This study also provides evidence that HIV infection was not specifically associated with oxidative stress among clinically stable individuals.

Adolescent↗
PubMed1999

Cerebrospinal fluid levels of selenium in patients with Alzheimer's disease.

We compared CSF and serum selenium levels, measured by atomic absorption spectrophotometry, in 27 patients with Alzheimer's disease (AD) (13 females, 14 males, mean +/- SD age 73.6 +/- 7.4 years) without major clinical signs of undernutrition, and 34 matched controls (18 females, 16 males, mean +/- SD age 70.7 +/- 7.8 years). CSF and serum selenium levels did not differ significantly between AD-patient (11.4 +/- 7.8 ng/ml and 28.5 +/- 13.0 ng/ml, respectively) and control groups (13.3 +/- 7.0 ng/ml and 22.5 +/- 17.5 ng/ml). These values were not correlated with age, age at onset, duration of the disease, and scores of the MiniMental State Examination in the AD group. Weight and body mass index were significantly lower in AD patients than in controls. These results suggest that CSF selenium concentrations are apparently unrelated with the reported oxidative stress processes in patients with AD.

Aged↗
PubMed1996

Micronutrients (vitamins and minerals) as cancer-preventive agents.

Reduction of incidence and mortality of common cancers requires successful preventive interventions both in high-risk populations and in the population at large. Agents chosen for intervention trials must have been demonstrated to have significant and plausible biological activity in animal, in vitro, and short-term human studies, and these should be supported by observational epidemiological analyses. This chapter reviews evidence about vitamins and minerals as possible cancer-protective agents, emphasizing carotenoids (notably beta-carotene), natural vitamin A, vitamin E, selenium, vitamin C, calcium, vitamin D and folic acid. It is helpful to group agents according to apparent primary mechanism of effect, such as antioxidant (and/or pro-oxidant) effects for beta-carotene, vitamin C, vitamin E, selenium, zinc, copper, iron, manganese, phenolic compounds and isothiocyanates. Certain conditions associated with increased concentrations of free radicals and reactive oxygen species-like smoking, aging and reduced glutathione levels-must be assessed as confounders. However, these chemicals generally have multiple effects, which also may complicate reliance on intermediate end points. To choose target populations, dosages and durations for interventions, it is essential to distinguish between overcoming a relative deficiency of the micronutrient in the diet and the circulation and providing a pharmacological dose. Selenium and beta-carotene are important examples of agents that may be protective at the high end of the normal diet-based distribution of serum values, but may be toxic-somehow-at much higher levels. We are becoming more aware that it is a long leap from associations observed or deduced in epidemiological studies to the design and demonstration of successful chemopreventive interventions with single agents or with combinations or mixtures. When interventions fail to support the hypotheses from observational epidemiology, it may be necessary to reconsider the hypotheses. Furthermore, effects may vary remarkably at different tumour sites.

Anticarcinogenic Agents↗
PubMed2004

Single-dose ebselen does not afford sustained neuroprotection to rats subjected to severe focal cerebral ischemia.

Oxygen free radicals have been involved in the pathophysiology of cerebral ischemia, especially after spontaneous or thrombolytic reperfusion. In this study with rats, we have combined a severe focal ischemic insult (2 h) and a prolonged reperfusion time (7 days) to assess the possible sustained neuroprotective effect of ebselen (10 or 100 mg/kg), a small, lipophilic organoselenium compound which mimics glutathione peroxidase. Parietal cortical perfusion was measured by laser-Doppler flowmetry, and focal cerebral ischemia was carried out by the intraluminal thread method. We have measured plasma selenium levels, brain reduced glutathione levels, as a marker of oxidative stress, and infarct volume associated with cerebral ischemia. Focal ischemia did not alter reduced glutathione levels, while 60 min reperfusion following ischemia induced a significant (P < 0.05) decrease in reduced glutathione levels of the ipsilateral hemisphere. Pretreatment with ebselen, which induced significant (P < 0.05) increase in plasma selenium levels, did not significantly alter the decrease in reduced glutathione levels. The ischemic insult induced 30% mortality on average, with deaths always occurring within 12-48 h. Surviving rats suffered up to 25% body weight loss 1 week after the ischemic insult. Infarct volumes were 26.8 +/- 4.7% of the hemisphere in placebo-treated rats, 26.6 +/- 3.6% in 10 mg/kg ebselen-treated rats, and 25.6 +/- 6.4% in 100 mg/kg ebselen-treated rats (not significantly different). Single-dose administration of ebselen does not reduce the size of brain infarct resulting from severe focal cerebral ischemia in rats. In contrast to previous studies with relatively earlier endpoints, we have delayed the measurement of infarct volume to 1 week after the ischemic insult.

Administration, Oral↗
PubMed1990

Ethanol-induced lipid peroxidation and oxidative stress in extrahepatic tissues.

An ethanol-induced oxidative stress is not restricted to the liver, where ethanol is actively oxidized, but can affect various extrahepatic tissues as shown by experimental data obtained in the rat during acute or chronic ethanol intoxication. Most of these data concern the central nervous system, the heart and the testes. An acute ethanol load has been reported to enhance lipid peroxidation in the cerebellum. This is accompanied by an increase in the cytosolic concentration of low-molecular-weight iron derivatives which may contribute to the generation of aggressive free radicals. The ethanol-induced decrease in the main antioxidant systems (superoxide dismutase, alpha-tocopherol, ascorbate and selenium) is a likely contributor to the cerebellar oxidative stress. Most of these disturbances can be prevented by allopurinol administration. Some experimental data support also the occurrence of pro- and anti-oxidant disturbances in the cerebellum and in other regions of the central nervous system after chronic ethanol administration. Chronic ethanol administration enhances lipid peroxidation in the heart. The increased conversion of xanthine dehydrogenase into xanthine oxidase as well as the activation of peroxisomal acyl CoA-oxidase linked to ethanol administration could contribute to the oxidative stress. Chronic ethanol administration elicits in the testes an enhancement in mitochondrial lipid peroxidation and a decrease in the glutathione level, which appear to be correlated to the gross testicular atrophy observed. Vitamin A supplementation attenuates the changes in lipid peroxidation, glutathione and testicular morphology. Whether the reported disturbances are involved in the pathogenesis of the tissue disorders observed in alcoholic patients remains unanswered.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1996

Inhibition of selenite-catalyzed superoxide generation and formation of elemental selenium (Se(o)) by copper, zinc, and aurintricarboxylic acid (ATA).

Selenite catalyzes the oxidation of glutathione (GSH) with the subsequent generation of superoxide (O2.-). Copper, zinc, and aurintricarboxylic acid (ATA) were tested for their ability to inhibit both the selenite-catalyzed generation of superoxide and the conversion of selenite to elemental selenium (Se(o)). As measured by lucigenin-dependent chemiluminescence (CL), copper, zinc, and ATA were shown to inhibit significantly (P < 0.05) selenite-catalyzed CL in a concentration-dependent manner. The inhibition of the selenium-catalyzed generation of superoxide by copper(II) was greater than by either zinc or ATA. In addition, Copper, zinc, and ATA all inhibited the conversion of selenite to Se(o). Inhibition of selenite-catalyzed CL by copper, zinc, and ATA is believed to occur as the result of inhibition of Se2- and/or GSSe-, the catalytic selenopersulfide anion of GSH.

Aurintricarboxylic Acid↗
PubMed1980

Influence of selenium, vitamin E, and ethoxyquin on lipid peroxidation in muscle tissues from fowl during low temperature storage.

The influences of various factors which affect the selenium-vitamin E status of laying hens on lipid peroxidation in muscle tissues during low temperature storage were studied. Laying hens from 32 to 56 weeks of age were fed low selenium and low vitamin E practical diets supplemented with different levels of Na2SeO3, d1-alpha-tocopherol acetate, ethoxyquin, and/or peroxidized corn oil. Vitamin E status as indicated by plasma vitamin E activity was improved by supplements of vitamin E, selenium, or ethoxyquin. Selenium status as indicated by plasma selenium-dependent glutathione peroxidase activity was improved by selenium supplementation. Incorporation of peroxidized corn oil into diets did not depress plasma vitamin E but increased plasma glutathione peroxidase when those diets contained supplemental selenium. Lipid peroxidation as indicated by the 2-thiobarbituric acid (TBA) method in muscle samples held at -20 C for up to 270 days was reduced by dietary selenium in M. pectoralis when corn oil was fed. Supplemental vitamin E or ethoxyquin reduced TBA values developed in M. gastrocnemius. Results indicate that dietary selenium and other factors affecting selenium status may be useful in retarding the development of oxidative rancidity in frozen poultry products.

Animals↗
PubMed1982

Characterization of the selenium-substituted 2 [4Fe-4Se] ferredoxin from Clostridium pasteurianum.

The sulfur atoms of the two [4Fe-4S] clusters present in the ferredoxin from Clostridium pasteurianum have been replaced by selenium. The substitution is readily carried out by incubating the apoferredoxin with excess amounts of Fe3+, selenite, and dithiothreitol under anaerobic conditions. The UV-visible absorption spectrum of the Se-substituted ferredoxin, the core extrusion of its active sites, and analyses of its iron and selenium contents show that it contains two [4Fe-4Se] clusters. The Se-substituted ferredoxin is considerably less resistant to oxygen or to acidic and alkaline pH than the native ferredoxin: the half-lives of the former are 20-500 times shorter than those of the latter. The native ferredoxin and the Se-substituted ferredoxin display similar kinetic properties when used as electron donors to the hydrogenase from C. pasteurianum. It is of note, however, that the Km and Vmax values are lower for the 2[4Fe-4Se] ferredoxin than for the 2[4Fe-4S] ferredoxin. Reductive and oxidative titrations with dithionite and with thionine, respectively, show that both ferredoxins are two-electron carriers. The redox potentials of the ferredoxins have been measured by equilibrating them with the H2/H+ couple via hydrogenase: values of -423 and -417 mV have been found for the 2[4Fe-4S] ferredoxin and 2[4Fe-4Se] ferredoxin, respectively. Ferredoxins containing both chalcogenides in their [4Fe-4X] (X = S, Se) clusters have been prepared by reconstitution reactions involving mixtures of sulfide and selenide: the latter experiments show that sulfide and selenide are equally reactive in the incorporation of [4Fe-4X] (X = S, Se) sites into ferredoxin. The present report, together with former studies, establishes the general feasibility of the Se/S substitution in [2Fe-2S] and in [4Fe-4S] clusters of proteins and of synthetic analogues.

Clostridium↗
PubMed2000

Reduction of the oxidative injury to the rabbits with established atherosclerosis by protein bound polysaccharide from Coriolus vesicolor.

Recent evidence has emerged that macrophage glutathione (GSH) content and selenium dependent glutathione peroxidase (SeGSHPx) activity are inversely related to cell-mediated oxidation of LDL, and intervention means to enhance the macrophage GSH-SeGSHPx status may contribute to attenuation of the atherosclerotic process. Our previous works showed that protein bound polysaccharide (PSK) injected intraperitoneally could enhance SeGSHPx activity and mRNA content of mouse macrophages. The aim of the present study is to demonstrate whether PSK can reduce the oxidative injury to the established atherosclerotic rabbits. Using the established atherosclerotic rabbit model, we studied the effect of PSK on oxidatively modified LDL (Ox-LDL), lipoperoxide (LPO) cholesterol contents and SeGSHPx activities of plasma and tissues (aorta, heart and liver) in the established atherosclerotic rabbits. As compared with the control group, Ox-LDL, LPO and cholesterol contents were much lower; SeGSHPx activities and SeGSHPx/LPO ratios were much higher in plasma and tissues (aorta, heart and liver); and the lesion area of aortae was reduced in the PSK group. Through the increment of SeGSHPx activity in macrophages and aortae, PSK enhances their antioxidation potentiality and improves the antioxidant/prooxidant imbalance in them, and thus decreases Ox-LDL, LPO and cholesterol contents of plasma and tissues, and regresses lesion area of aortae in the established atherosclerotic rabbits.

Animals↗
PubMed1996

Selenium-containing compounds protect DNA from single-strand breaks caused by peroxynitrite.

Peroxynitrite (ONOO-/ONOOH) is a powerful oxidant that can induce mutations and cause single-strand breaks in plasmid supercoiled DNA. The selenium-containing compound ebselen rapidly reacts with peroxynitrite. Therefore, ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one] and other selenium-containing molecules, selenomethionine and selenocystine, were studied as agents protecting DNA from single-strand breaks induced by peroxynitrite. Selenomethionine and selenocystine protected DNA from single-strand breaks more effectively than their sulfur analogs, methionine and cystine, and they also were more effective than glutathione or the hydroxyl radical scavenger mannitol. These results suggest that selenium-containing compounds can protect DNA from damage caused by peroxynitrite.

Cystine↗
PubMed1997

Phospholipid hydroperoxide glutathione peroxidase (PHGPx): more than an antioxidant enzyme?

The family of glutathione peroxidases encompasses, as far, three tetrameric glutathione peroxidases (GPx) and the monomeric PHGPx. Although the overall homology between tetrameric enzymes and PHGPx is less than 30%, a pronounced similarity has been detected on clusters involved in the active site and a common catalytic triad (selenocysteine glutamine and tryptophan) has been defined by structural and kinetic data. A major peculiar feature of the reaction catalyzed by PHGPx is the possibility to accommodate large lipophilic substrates. This accounts for the observed dramatic antiperoxidant effect and the synergism with vitamin E. Moreover, the reduction of lipid hydroperoxides accounts also for the observed modulation of cycloxygenase and inhibition of 15-lipoxygenase. On the other hand, structural and kinetic data indicate that also the specificity of PHGPx for the donor substrate is not restricted to GSH and the recent observation the PHGPx binds to specific mitochondrial proteins, from which it is released by ionic strength and thiols, suggests a possible fole of this selenoenzyme in catalyzing the specific oxidation of protein thiols, thus modulating the activity of cellular regulatory elements. On this light, the selenium mojety of PHGPx, reacting much faster that thiols with a peroxide, and then oxidizing specific protein thiols, would channel the oxidation toward protein targets, thus providing, by protein-protein interaction, the specificity of the redox transition.

Animals↗
PubMed2001

Role of some trace metal ions in placental membrane lipid peroxidation.

The antioxidative and/or pro-oxidative potential of three trace metal ions, namely aluminum (Al), manganese (Mn), and selenium (Se), has been studied. The effect of Al and Mn was found to be anion independent. The pro-oxidative potential of Al was more prominent than its antioxidative potential. This may be due to its redox inert nature. The increase in lipid peroxidation rates in placental syncytiotroblast membranes may contribute to the etiology of aluminum toxicity. Selenium had an antioxidative potential only in the whole-cell homogenate. This appears to be mediated by glutathione peroxidase of which Se is a cofactor. Manganese proved to be the trace metal ion of choice. It decreased the production of thiobarbituric acid reactive substances (TBARS). This may be due to its capacity to quench the superoxide anion and hydroxyl radicals and also due to its chain-breaking capacity. During the present course, ferrous-ascorbate mediated lipid peroxidation has been studied using various combinations of FeSO4 and ascorbic acid. Extrapolating the combined ratio of the individual combination as substrate concentration ([S]) and treating the observed amount of malondialdehyde (MDA) produced equivalent to initial velocity (vi), as in the case of enzymatic studies, the data were treated according to Michaelis-Menten kinetics and the values of kc and Cmax have been calculated.

Alkaline Phosphatase↗
PubMed1996

Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats.

The stimulation of thyroid hormone synthesis in iodine deficiency may increase the requirement for the selenoproteins which are involved in thyroid hormone synthesis in the thyroid gland. Selenoenzyme activity and expression were investigated in the thyroid and liver of second generation selenium-and/or iodine-deficient rats. Selenium deficiency caused substantial decreases in hepatic selenium-containing type I iodothyronine deiodinase (ID-I) and cytosolic glutathione peroxidase (cGSHPx) activities and mRNA abundances, but phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activity was only 55% of selenium-supplemented control levels, despite the absence of change in its mRNA abundance. Selenoenzyme mRNA concentrations were maintained at control levels in thyroid glands from the selenium-deficient rat pups. Despite this, a differential effect was observed in selenoenzyme activities: ID-I activity was decreased to 61%, cGSHPx activity to 45% and phGSHPx to 29% of that in selenium-adequate controls. In iodine-deficient thyroid glands, mRNA levels were increased 2.2, 5.0 and 2.8 times for ID-I, cGSHPx and phGSHPx respectively. ID-I and cGSHPx enzyme activities were also increased but the activity of phGSHPx was decreased despite the high mRNA abundance. Thyroid selenoprotein mRNA levels were also increased in combined selenium and iodine deficiency but again there were differential effects on enzyme activities, with ID-I activity increased, cGSHPx unchanged and phGSHPx decreased. Thus, iodine deficiency may produce an oxidant stress on the thyroid gland, increasing the requirement for selenium to maintain selenoenzyme activity. When dietary supplies of selenium are limiting, thyroid selenoprotein mRNA levels are increased to compensate for overall lack of the micronutrient. Furthermore, there is a preferential supply of available selenium to ID-I and cGSHPx to allow maintenance of thyroid function.

Aging↗
PubMed2006

Microbial selenate sorption and reduction in nutrient limited systems.

In this study, batch sorption experiments and X-ray adsorption spectroscopy (XAS) were utilized to investigate selenate sorption onto Shewanella putrefaciens 200R. Selenate sorption was studied as a function of pH (ranging from 3 to 7), ionic strength (ranging from 0.1 to 0.001 M), and initial selenate concentration (ranging from 10 to 5000 microM) in the absence of external electron donors. The results show that the extent of selenate sorption is strongly dependent on pH and ionic strength, with maximum sorption occurring at low pH (pH = 3) and low ionic strength (0.001 M NaCl) conditions. The strong dependence of Se sorption with ionic strength suggests the formation of outersphere complexes with the cell wall functional groups. Langmuir isotherm plots yielded log Kads values from 2.74 to 3.02. Desorption experiments demonstrated thatthe binding of selenate onto S. putrefaciens was not completely reversible. XANES analysis of the cells after sorption experiments revealed the presence of elemental selenium, indicating that S. putrefaciens has a capacity to reduce Se(VI) to Se(0) in the absence of external electron donors. We conclude that Se sorption onto S. putrefaciens cell walls is the result of the combination of outer-sphere complexation and cell surface reduction. This sorption process leads to a complex reservoir of bound Se which is not entirely reversible.

Adsorption↗
PubMed2006

Role of selenium supplementation and heat stress on trehalose and glutathione content in Saccharomyces cerevisiae.

The role of selenium (Se) supplementation on glutathione, a potent intracellular redox buffer, and trehalose, a well-known stress protectant molecule, was studied. The amount of glutathione decreased significantly while that of trehalose showed a minor decrease in the cells grown in Se-supplemented medium. After heat shock, glutathione content diminished further, whereas that of trehalose increased significantly in control and Se-supplemented cells. These findings suggest the importance of trehalose as an antioxidant molecule.

Glutathione↗