Effects of low selenium diets on antioxidant status and MPTP toxicity in mice

To investigate the role of chronic oxidative stress in MPTP neurotoxicity, C57BL mice were maintained 6–8 weeks on diets deficient in nutrients essential to cellular antioxidant defenses, selenium (Se) and alpha-tocopherol (vit E), and the effects on tissue antioxidant status and MPTP toxicity were evaluated relative to controls on supplemented diets. Activities of the major antioxidant enzymes, glutathione peroxidase (GPx), catalase, and superoxide dismutase, and levels of malondialdehyde as a marker for oxidative stress, were measured in brain, lung, liver and blood. Caudate depletion of dopamine and its metabolites served as a measure of MPTP neurotoxicity. For mice on the Se deficient diet, levels of the selenoenzyme GPx decreased from 50% in brain to 90% in blood. No compensatory changes in the activities of the other antioxidant enzymes were observed and addition of vit E to the diet did not alter antioxidant enzyme activities or malondialdehyde levels. In animals not treated with MPTP, the Se deficient diet significantly increased malondialdehyde only in liver. No protective effect of the antioxidant supplements against caudate depletion of dopamine and its metabolites was observed. However, malondialdehyde levels were increased in the brains of MPTP treated mice on the low Se diets, suggesting the possibility of secondary oxidative damage to tissues accompanying the destruction of substantia nigra neurons by MPTP.     

Effect of dietary selenium on the promotion of hepatocarcinogenesis by 3,3', 4,4'-tetrachlorobiphenyl and 2,2', 4,4', 5,5'-hexachlorobiphenyl

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that have promoting activity in the liver. PCBs induce oxidative stress, which may influence carcinogenesis. Epidemiological studies strongly suggest an inverse relationship between dietary selenium (Se) and cancer. Despite evidence linking Se deficiency to hepatocellular carcinoma and liver necrosis, the underlying mechanisms for Se cancer protection in the liver remain to be determined. We examined the effect of dietary Se on the tumor promoting activities of two PCBs congeners, 3,3', 4,4'-tetrachlorobiphenyl (PCB-77) and 2,2', 4,4', 5,5'-hexachlorobiphenyl (PCB-153) using a 2-stage carcinogenesis model. An AIN-93 torula yeast-based purified diet containing 0.02 (deficient), 0.2 (adequate), or 2.0 mg (supplemental) selenium/kg diet was fed to Sprague-Dawley female rats starting ten days after administering a single dose of diethylnitrosamine (150 mg/kg). After being fed the selenium diets for 3 weeks, rats received four i.p. injections of either PCB-77 or PCB-153 (150 micromol/kg) administered every 14 days. The number of placental glutathione S-transferase (PGST)-positive foci per cm(3) and per liver among the PCB-77-treated rats was increased as the Se dietary level increased. Unlike PCB-77, rats receiving PCB-153 did not show the same Se dose-response effect; nevertheless, Se supplementation did not confer protection against foci development. However, the 2.0 ppm Se diet reduced the mean focal volume, indicating a possible protective effect by inhibiting progression of preneoplastic lesions into larger foci. Cell proliferation was not inhibited by Se in the liver of the PCB-treated groups. Se did not prevent the PCB-77-induced decrease of hepatic Se and associated reduction in glutathione peroxidase (GPx) activity. In contrast, thioredoxin reductase (TrxR) activity was not affected by the PCBs treatment or by Se supplementation. These findings indicate that Se does not inhibit the number of PGST-positive foci induced during promotion by PCBs, but that the size of the lesions may be inhibited. The effects of Se on altered hepatic foci do not correlate with its effects on GPx and TrxR.     

Role of Synthesized Organoselenium Compounds on Protection of Rat Erythrocytes from DMBA-Induced Oxidative Stress

Formation of free radicals is not limited to normal cellular process but also occur upon exposure to certain chemicals (polycyclic aromatic hydrocarbon, cadmium, lead, etc.), cigarette smoke, radiation, and high-fat diet. Free-radical damage is an important factor in many pathological and toxicological processes. Selenium, an essential micronutrient, is a associated with antioxidant functions, physiological defense mechanisms against different diseases including several types of cancers. Search for new selenium compounds with more chemopreventive activities and less toxicities are in progress. In addition, there has been a growing interest in the synthesis of organoselenium compounds with respect to their use in enzymology and bioorganic chemistry. In the present study, adult female Wistar rats were treated with 7,12-dimethylbenz[a]anthracene (DMBA) and the organoselenium compounds [1-isopropyl-3-methylbenzimidazole-2-selenone (Se I) and 1, 3-di-p-methoxybenzylpyrimidine-2-selenone (Se II)] in determined doses. The protective effects of synthetic organoselenium compounds (Se I and Se II) against DMBA-induced changes in antioxidant enzyme (superoxide dismutase, glutathione peroxidase (GSH-Px), catalase (CAT), glutathione reductase (GR)) activities, total GSH, and malondialdehyde (MDA) levels of rat erythrocyte were investigated. The DMBA-treated group exhibited significant decreases in the levels of erythrocyte GSH-Px, CAT, and GR activities, an increase in MDA levels, and a decrease in total GSH level compared to the control. Se I and Se II fully or partially restored enzyme activity. Lipid peroxidation was also decreased in Se-I- and Se-II-treated groups.     

Effect of selenium on N-nitrosodiethylamine-induced multistage hepatocarcinogenesis with reference to lipid peroxidation and enzymic antioxidants

We have studied the relationship between antioxidant and anticancer properties of selenium (Se) in multistage hepatocarcinogenesis induced by N-nitrosodiethylamine (DEN). In this study we have observed an increased level of lipid peroxide (LPO) products and decreased antioxidant enzyme activities (superoxide dismutase and catalase) in hepatoma and surrounding liver tissues of cancer-bearing animals. Selenium (Se) was supplemented either before initiation or during initiation and selection/promotion phases of hepatocarcinogenesis and was found to be effective in altering hepatic lipid peroxidation and antioxidant enzyme activities to a statistically significant level measured either in the hepatoma or in the surrounding liver tissues. These alterations inclined towards normal in a time-dependent manner on selenium supplementation. Furthermore, increased levels of lipid peroxidation and decreased levels of antioxidants (superoxide dismutase and catalase) were also observed in distant organs of cancer-bearing rats other than the tumour-bearing site. These alterations are brought back to normal levels upon Se treatment. Our results confirm the fact that Se is particularly protective in limiting the action of DEN by its antioxidant property.     

Investigation of lipid peroxide and glutathione redox status of chicken concerning on high dietary selenium intake

This study was designed to investigate the effects of excess (24.5 mg Se/kg feed) inorganic and organic dietary selenium supplementation on 3-week-old broilers. The experiments lasted 4 days. Intensity of lipid peroxidation processes (malondialdehyde, MDA) and the amount (reduced glutathione, GSH) and activity (glutathione peroxidase activity, GSHPx) of gluathione redox system were measured in blood plasma, red blood cell hemolysate and liver. Voluntary feed intake in the selenium-treated groups reduced remarkably. Elevated GSH concentration and GSHPx activity were measured in plasma and liver of both selenium-treated groups compared to the untreated control and the 'pair-fed' controls. The lipid peroxidation processes in the liver showed higher intensity than the control due to both selenium treatment. The applied dose of selenite and selenomethionine does not inhibit, but even improves the activity of glutathione redox system in the liver during the early period of selenium exposure.     

Elevation of thiobarbituric acid values in the rat liver intoxicated by T-2 toxin

In the present study we first demonstrated that T-2 toxin markedly stimulated lipid peroxidation specifically in the liver of rats. The amount of lipid peroxides in the liver, estimated by the thiobarbituric acid (TBA) method, increased dose dependently, being proportional to the extent of its acute toxicity measured by various parameters in rats fed a commercial diet. Further, to elucidate the mechanism of lipid peroxidation and its role in hepatic injury caused by T-2 toxin, time-course studies on the correlation between lipid peroxide content and some biological and histopathological data were undertaken in rats given 4 mg of the toxin/kg perorally. The TBA reactive substances in the liver began to increase after 6 hr. However, much earlier than this there were some other alterations, which included decreases in the amount of cytochrome P-450 in the liver, of GPT (thereafter an increase) and phospholipids in the plasma, and of basophilic masses in the hepatocytes (arrayed as a rough endoplasmic reticulum in the electron micrograph). The vitamin E-deficient study showed that vitamin E markedly inhibited the stimulative effect of T-2 toxin on lipid peroxidation, but not diminish any other measured parameters of the injury. The toxin-induced stimulation of lipid peroxidation does not appear to be caused by activation of microsomal NADPH-cytochrome c reductase nor by a decrease in the level of cytosolic glutathione peroxidase. These results suggest that T-2 toxin might induce some alteration of the membrane structure and consequently might stimulate lipid peroxidation in situ.     

Zinc Deficiency and Oxidative Stress Involved in Valproic Acid Induced Hepatotoxicity: Protection by Zinc and Selenium Supplementation

Valproic acid (VPA) is an antiepileptic drug, which its usage is limited due to its hepatotoxicity. The present study was conducted to investigate the efficacy of zinc (Zn) and selenium (Se), necessary trace elements, against VPA-induced hepatotoxicity in Wistar rats. The animals were divided into five groups: control, VPA 200 mg/kg, VPA + Zn (100 mg/kg), VPA + Se (100 mg/kg), and VPA + Zn + Se. The administration of VPA for four consecutive weeks resulted in decrease in serum level of Zn in rats. Also, an increase in liver marker enzymes (ALT and AST) and also histological changes in liver tissue were shown after VPA administration. Oxidative stress was evident in VPA group by increased lipid peroxidation (LPO), protein carbonyl (PCO), glutathione (GSH) oxidation, and reducing total antioxidant capacity. Zn and Se (100 mg/kg) administration was able to protect against deterioration in liver enzyme, abrogated the histological change in liver tissue, and suppressed the increase in oxidative stress markers. Zn and combination of Zn plus Se treatment showed more protective effects than Se alone. These results imply that Zn and Se should be suggested as effective supplement products for the prevention of VPA-induced hepatotoxicity.     

Effect of 4-week feeding of deoxynivalenol- or T-2-toxin-contaminated diet on lipid peroxidation and glutathione redox system in the hepatopancreas of common carp (<Emphasis Type="Italic">Cyprinus carpio</Emphasis> L.)

The purpose of study was to investigate the effects of T-2 toxin (4.11 mg T-2 toxin and 0.45 mg HT-2 toxin kg^?1 feed) and deoxynivalenol (5.96 and 0.33 mg 15-acetyl deoxynivalenol (DON)?kg^?1 feed) in 1-year-old common carp juveniles in a 4-week feeding trial. The exposure of mycotoxins resulted in increased mortality in both groups consuming mycotoxin-contaminated diet. Parameters of lipid peroxidation were not affected during the trial, and antioxidant defence also did not show response to oxidative stress; however, glutatione peroxidase activity slightly, but significantly, decreased in the T-2 toxin group. Glutathione S-transferase activity showed moderate decrease as effect of T-2 toxin, which suggests its effect on xenobiotic transformation. Reduced glutathione concentration showed moderate changes as effect of DON exposure, but T-2 toxin has no effect. Expression of phospholipid hydroperoxide glutathione peroxidase (GPx4) genes showed different response to mycotoxin exposure. T-2 toxin caused dual response in the expression of gpx4a (early and late downregulation and mid-term upregulation), but continuous upregulation was found as effect of deoxynivalenol. Expression of the other gene, gpx4b, was upregulated by both trichothecenes during the whole period. The results suggested that trichothecenes have some effect on free radical formation and antioxidant defence, but the changes depend on the duration of exposure and the dose applied, and in case of glutathione peroxidase, there was no correlation between expression of genes and enzyme activity.     

Properties of glutathione peroxidase from the hepatopancreas of freshwater prawn Macrobrachium malcolmsonii

Oxidative stress stimulates production of hydrogen peroxide and organic hydroperoxides which are involved in lipid peroxidation and oxidative damage to protein. Glutathione peroxidase protects against oxidative stress. Quantitative data on glutathione peroxidase of crustaceans are very limited and so this study was performed to determine the assay condition of glutathione peroxidase in crustaceans. Particularly, some properties of hepatic selenium dependent glutathione peroxidase and total glutathione peroxidase of the freshwater prawn Macrobrachium malcolmsonii were examined. The optimal pH for Se-GSH-Px was 7.5 and for total GSH-Px was 8.0. The activation energy (E_a) was found to be 9.14 Kcal/mol for Se-GSH-Px and 10.96 Kcal/mol for total GSH-Px. The energy inhibition (E_i) value for Se-GSH-Px was 14.36 Kcal/mol and 13.71 Kcal/mol for total GSH-Px. The Km values were also determined at various concentrations of substrates (GSH, CHP, H₂O₂) for both enzymes.     

Organoselenium (Sel-Plex diet) decreases amyloid burden and RNA and DNA oxidative damage in APP/PS1 mice

To evaluate potential antioxidant characteristics of organic selenium (Se), double knock-in transgenic mice expressing human mutations in the amyloid precursor protein (APP) and human presenilin-1 (PS1) were provided a Se-deficient diet, a Se-enriched diet (Sel-Plex), or a control diet from 4 to 9 months of age followed by a control diet until 12 months of age. Levels of DNA, RNA, and protein oxidation as well as lipid peroxidation markers were determined in all mice and amyloid β-peptide (Aβ) plaques were quantified. APP/PS1 mice provided Sel-Plex showed significantly (P < 0.05) lower levels of Aβ plaque deposition and significantly decreased levels of DNA and RNA oxidation. Sel-Plex-treated mice showed no significant differences in levels of lipid peroxidation or protein oxidation compared to APP/PS1 mice on a control diet. To determine if diminished oxidative damage was associated with increased antioxidant enzyme activities, brain glutathione peroxidase (GSH-Px), glutathione reductase, and glutathione transferase activities were measured. Sel-Plex-treated mice showed a modest but significant increase in GSH-Px activity compared to mice on a normal diet (P < 0.5). Overall, these data suggest that organic Se can reduce Aβ burden and minimize DNA and RNA oxidation and support a role for it as a potential therapeutic agent in neurologic disorders with increased oxidative stress.     

Protective effects of selenium against cadmium induced hematological disturbances,immunosuppressive, oxidative stress and hepatorenal damage in rats

Cadmium is a non-essential toxic metal used in industrial process, causes severe risk to human health. Selenium (Se) is an essential trace mineral of fundamental importance for human health. Selenium has antioxidant enzymes roles and is needed for the proper function of the immune system. In this study, the protective effects of selenium against cadmium intoxication in rats have been investigated by monitoring some selective cytokines (IL-1β, TNF α, IL-6, IL-10 and IFN-γ), antioxidant enzymes reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and lipid peroxidation malondialdehyde (MDA) as well as some selective biochemical markers of liver and kidney functions. Thirty-two rats were divided into four equal groups; the first group was used as a control. Groups 2–4 were treated with selenium (Se; 0.1 mg/kg BW), cadmium (Cd; 40 mg/L drinking water) and selenium plus cadmium, respectively. Rats were orally administered their relevant doses daily for 30 days. Blood samples were collected from heart puncture at the end of the experiment (30 days) for complete blood picture (CBC) and serum was separated to evaluate the different immunological parameters and biochemical parameters, as well as liver specimens for Cd and Se estimation. Rats in the Cd treated group have a significantly higher hepatic concentration of Cd than in other treated groups. Results revealed that cadmium significantly increased IL-1β, TNF α, IL-6 and IL-10, beside peripheral neutrophils count, while the IFN-γ and lymphocytes were decreased in rat sera. In addition, GSH level, CAT, SOD and GPx activities were significantly decreased while lipid peroxidation (MDA) was increased. Regarding, liver and renal markers, they were significantly increased in the activities of aminotransferases (AST, ALT), urea and creatinine, while total plasma proteins and albumin were significantly decreased. On the other hand, selenium treated group, showed significantly increased IFN-γ, GSH level, CAT, and GPx activities, as well as lymphocyte count while IL-10 was decreased. Selenium in combination with cadmium, significantly improved the elevation of serum IL-1β, IL-6, TNF α, IL-10 and malondialdehyde in addition to enhancing the antioxidant enzyme activities of GSH, CAT, GPx and SOD. Moreover, selenium has ameliorated the cadmium-induced liver and kidney damage by improving hepatic and renal markers. The results of this investigation demonstrated that selenium has the potential to countermeasure the immunosuppressive as well as hepatic and renal oxidative damage induced by cadmium in rats; selenium has shown promising effects against Cd toxicity.     

Glutathione Peroxidase Activity and Erythrocyte Lipid Peroxidation as Indices of Selenium and Vitamin E Status in Young Pigs

A randomized, blocked 23 factorial experiment was conducted with 48 pigs from sows fed a diet low in selenium and vitamin E. From 3 to 12 weeks of age the piglets were kept in single pens and fed a basic diet consisting mostly of barley, dried skim milk, soybean meal and dried yeast, and containing 55 µg selenium and 3 mg vitamin E per kg. The treatment factors — i.e. feed supplements — were 2 levels of Se (nil, 60 µg/kg), 2 levels of vitamin E (nil, 50 mg/kg), and 2 levels of the feed antioxidant ethoxyquin (nil, 150 mg/kg). Blood samples, collected at termination of the experiment, were examined for glutathione peroxidase activity (GSH-Px) and resistance against erythrocyte lipid peroxidation (ELP) to evaluate Se and vitamin E status, respectively. Analysis of variance showed the GSH-Px activity to be litter-dependent (P < 0.001) and influenced by selenium supplementation (P < 0.001) but not by the other supplements or by interactions between supplements. Resistance against ELP was influenced only by vitamin E supplementation (P < 0.001). GSH-Px and ELP thus seem to be valuable and simple methods for evaluating, respectively, Se status and vitamin E status in growing pigs.     

Elevation of rat liver mRNA for selenium-dependent glutathione peroxidase by selenium deficiency.

Selenium-dependent glutathione peroxidase (Se-GSH-Px, GSH-H2O2 oxidoreductase EC 1.11.1.9) is the best characterized selenoprotein in higher animals, but the mechanism whereby selenium becomes incorporated into the enzyme protein remains under investigation. To elucidate the mechanism of insertion of selenium into Ge-GSH-Px further, we have systematically analyzed and compared the results of Western blot, in vitro translation immunoprecipitation, and Northern blot experiments conducted with liver proteins and RNAs obtained from rats fed on selenium-deficient and selenium-supplemented diets. The anti-serum employed in this study was raised against an electrophoretically pure Se-GSH-Px preparation obtained from rat livers by a simplified purification procedure involving separation by high performance liquid chromatography on a hydrophobic interaction column. Different forms of Se-GSH-Px, including apo-protein, cross-reacted with this antiserum and Western blot analysis found no Se-GSH-Px protein present in livers from rats fed on selenium-deficient diets. By contrast, a distinct protein band corresponding to purified Se-GSH-Px was detected in livers from selenium-supplemented animals, a result consistent with the finding that the Se-GSH-Px activity was reduced to undetectable levels in livers of selenium-deficient rats. The in vitro translation experiments, however, indicated not only that mRNA for Se-GSH-Px was present during selenium deficiency but also that its translation products contained 2-3-fold as much immunoprecipitable protein as the products of poly(A) RNA from livers of selenium-supplemented rats. This result suggests that the Se-GSH-Px mRNA may be increased in the selenium-deficient state. Elevated levels of Se-GSH-Px mRNA were directly demonstrated in Northern blot experiments employing cDNA clone pGPX1211 as a probe. A similar increase in Se-GSH-Px mRNA was observed in such other tissues as kidney, testis, brain, and lung tissue, in selenium-deficient states. The present data support the co-translational mechanism for the incorporation of selenium into Se-GSH-Px in rat liver.     

Effect of vitamin E and selenium on antioxidant enzymes in brain,kidney and liver of cigarette smoke-exposed mice

The present study was conducted to evaluate the protective effects of vitamin E and selenium (Se) application on alteration of antioxidant enzyme activities against cigarette smoking induced oxidative damage in brains, kidneys and liver of mice. Male mice (balb/c) were exposed to cigarette smoke and treated with Se and/or vitamin E. Glutathione transferase (GST), glutathione peroxidase (GPX), glutathione reductase (GRX), superoxide dismutase (SOD) and catalase (CAT) enzyme activities in mice brain, kidney and liver were measured spectrophotometrically. GST, GPX, GRX, SOD and CAT enzyme activities in the brains of smoke-exposed mice were found lower than the enzymes activities of control mice and Se-and vitamin E-treated mice at the end of the three and five months. Opposite to brain, enzyme activities in kidneys and livers of smoke-exposed mice were found higher than the enzymes activities of control mice and Se-and vitamin E-treated mice at the end of the three and five months. Activities of GST, GPX, GRX SOD and CAT in the livers, kidneys and brains of smoke-exposed mice were found statistically different (p < 0.01) compared to control mice and Se-and vitamin E-treated mice. Combined application of vitamin E and Se had an additive protective effect against changing enzymes activities in smoke-exposed mice livers, kidneys and brains at the end of the both application periods. These results suggest that cigarette smoke exposure enhances the oxidative stress, thereby disturbing the tissue antioxidant defense system and combined application of vitamin E and Se protects the brain, kidney and liver from oxidative damage through their antioxidant potential.     

Roles of antioxidants on prolonged storage of avian spermatozoa in vivo and in vitro

This review focuses on natural and assisted prevention against lipid peroxidation in avian spermatozoa. The presence of high levels of n-6 polyunsaturated fatty acids (PUFAs) in the plasma membrane creates favorable conditions for the formation of peroxidative products, a major cause of membrane damage which may ultimately impair male fertility. However, a complex antioxidant system involving vitamin C, vitamin E and GSH is naturally present in avian semen. Coupled with a battery of enzymatic defenses (e.g., SOD, GSH-Px either Se- or non-Se-dependent), this system acts to prevent or restrict the formation and propagation of peroxides. The presence of specialized sites dedicated to prolonged sperm storage in avian females raises the question of durable protection of sperm membranes against peroxidation. Preliminary observations have revealed the presence of a specific antioxidant system at these sites in which vitamin C could exert a major role. From a practical standpoint, the extensive use of artificial insemination in poultry, along with the emergence in some species of workable techniques to cryopreserve spermatozoa, demand better control of peroxidation occurring in the plasma membrane of spermatozoa before or during storage. Dietary supplementation with vitamin E is effective in limiting lipid peroxidation of sperm plasma membranes, both in chickens and turkeys. In addition, organic Se with or without vitamin E stimulates Se-GSH-Px activity in seminal plasma. Preliminary observations in female chickens have also revealed the effectiveness of dietary supplementation with vitamin E, organic selenium or both to sustain fertility in aging flocks.     

Lipid peroxidation and glutathione system in hyperlipemic rabbits: influence of olive oil administration

We studied the effect of supplementation (10% w/w) of a hyperlipemic diet (1% cholesterol) with olive oil (OLIV) for 6 weeks in four groups of 10 rabbits each. At the end of this period, we determined lipid peroxidation, glutathione content, and glutathione peroxidase, reductase and transferase activities in liver, brain, heart, aorta and platelets. The atherogenic diet increased tissue lipid peroxidation and decreased the protective antioxidant effect of glutathione. Dietary supplementation with olive oil reduced tissue lipid peroxidation by 71.6% in liver, 20.3% in brain, 84.5% in heart, 63.6% in aorta, 72% in platelets. The ratios total/oxidized glutathione were increased in all tissues (49% in liver, 48% in brain, 45% in heart, 83% in aorta, 70% in platelets). Olive oil increased glutathione peroxidase and transferase activities in all tissues. We conclude that in rabbits made hyperlipemic with a diet rich in saturated fatty acids, olive oil decreased tissue oxidative stress.     

Wheat bran protects Fischer-344 rats from diquat-induced oxidative stress by activating antioxidant system: selenium as an antioxidant

Wheat bran had a protective effect against diquat toxicity in rats fed a purified diet (PD). We studied the effects of wheat bran on the antioxidant system in the liver of rats treated with saline and diquat. Although feeding wheat bran did not affect the concentration of hepatic non-protein sulfhydryl or the activity of glucose 6-phosphate dehydrogenase in the saline-injected rats, these values were significantly higher in the rats fed PD containing wheat bran (W-PD) than in rats fed only PD after administering diquat. The glutathione peroxidase and reductase activities were significantly elevated by wheat bran in the saline-injected rats. Although the glutathione peroxidase activity was unchanged in both the PD-fed rats and W-PD-fed rats after the diquat treatment, the glutathione reductase activity was significantly decreased in both the PD-fed and W-PD-fed rats. Feeding the rats with PD containing 0.15 ppm selenium as well as with W-PD elevated the activity of hepatic glutathione peroxidase and attenuated the diquat toxicity. These results indicate that wheat bran protected against diquat toxicity by activating the hepatic antioxidant system, and that selenium was the key antioxidant in wheat bran.     

Selenium and Vitamin E Modulates Cigarette Smoke Exposure-Induced Oxidative Stress in Blood of Rats

Cigarette smoke contains about 5,000 chemicals that include organic and metallic compounds. The current study was undertaken to investigate the effects of selenium and vitamin E on oxidative stress-induced damage in rats exposed to cigarette smoke. Forty male rats were equally divided into four groups. The first and second groups were used as control and cigarette smoke groups, respectively. Selenium was administered to rats constituting the third group for 27 days. The Se and vitamin E combination was given to animals in fourth group for 27 days. All groups except the control, were exposed to cigarette smoke starting at the third day of the experiment and continuing for 27 days. The blood samples from all groups were taken at the end of 27 days. Plasma lipid peroxidation, triacylglycerol, and total cholesterol levels were higher in the cigarette smoke group than in the control, although erythrocytic superoxide dismutase and glutathione peroxidase activities were lower in the cigarette smoke group than in the control. The plasma lipid peroxidation, triacylglycerol, and total cholesterol levels were lower in cigarette smoke+Se+VE group than in the cigarette smoke group, although erythrocytic superoxide dismutase activity and glutathione peroxidase activity in selenium and vitamin E-administered groups were higher than in the exposed to cigarette smoke group. High-density lipoprotein-cholesterol level was not affect by selenium and vitamin E administrations. In conclusion, selenium and vitamin E seem to have protective effects on the cigarette smoke-induced blood toxicity by supporting the enzymatic antioxidant redox systems.     

Optimization of selenium status by a single intraperitoneal injection of Se in Se-deficient rat: possible application to burned patient treatment

In order to investigate the efficiency of a single selenium (Se) administration in restoring selenium status, Se and antioxidant enzymes were studied in an animal model of Se depletion. In Se-depleted animals receiving or not a single parenteral administration of Se, plasma, red blood cell (RBC), and tissue Se levels were measured concurrently with glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities. The oxidative stress was assessed by thiobarbituric acid-reactive species (TBARs), total thiol groups, glutathione, and tocopherol measurements. Our study showed that Se depletion with alterations in the antioxidant defense system (Se and GPx activity decreases) led to an increase of lipid peroxidation, a decrease of the plasma vitamin E level, and SOD activation. Sodium selenite injection resulted after 24 h in an optimal plasma Se level and a reactivation of GPx activity. In liver, brain, and kidney, Se levels in injected animals were higher than those in reference animals. However, this single administration of Se failed to decrease free radical damage induced by Se depletion. Therefore, in burned patients who exhibit an altered Se status despite a daily usually restricted Se supplementation, the early administration of a consistent Se amount to improve the GPx activity should be of great interest in preventing the impairment of the antioxidant status.