Antioxidant Effects Of Selenium Research Articles

Experimental study of the antioxidant and antidiabetic effects of a colloid nanosized selenium solution

Oxidative stress resulting from an imbalance of free radical oxidation (FRO) and antioxidant defense (AOD) is one of the main pathogenetic processes underlying the development of type 1 diabetes mellitus (DM1) and its complications. The purpose of the study was to reveal the ability of a colloidal nanosized selenium solution to correct the indices of FRO and AOD in rats when modeling alloxan DM1. Materials and methods. The experiment was carried out on male Wistar rats divided into groups: intact, control (healthy rats treated with selenium); DM1; DM1 treated with selenium. DM1 was simulated by intraperitoneal injection of an alloxan solution at a dose of 170 mg/kg. A solution of selenium was administered intragastrically to diabetic and control rats at a dose of 46.7 μg/kg three times a week (12 injections). A colloidal solution of nanosized selenium was obtained by laser ablation using radiation of two wavelengths. In blood plasma were determined: the content of glucose, urea, creatinine, total protein, reduced glutathione, and malondialdehyde; activity of aminotransferases (AST, ALT), α-amylase, alkaline phosphatase; in whole blood — the content of glycated hemoglobin (HbA1c); in hemolysate of erythrocytes — the activity of superoxide dismutase (SOD), catalase, glutathione peroxidase. Results and discussion. Modeling of alloxan diabetes mellitus is accompanied by the development of hyperglycemia and changes in biochemical parameters indicating damage to liver cells (ALT), kidneys (urea, creatinine), myocardium (AST), and the development of oxidative stress (accumulation of malondialdehyde), partially compensated by SOD activation. The antidiabetic effect of selenium solution is manifested in the correction of glucose and HbA1c levels, liver and kidney profile indicators. The antioxidant effect of selenium is manifested in the normalization of the level of malondialdehyde and in reducing the need for reduced glutathione. The administration of selenium to healthy animals is accompanied by an increase in indicators reflecting the stressful effect of intragastric administration procedures (glucose, SOD) and, possibly, the toxic effect of selenium nanoparticles, which requires a more detailed study. Conclusion. A colloidal solution of nanosized selenium, obtained by an original method, had an antioxidant and antidiabetic effect on rats with type 1 alloxan diabetes mellitus.

Anti-inflammatory and Antioxidant Effects of Selenium on Orbital Fibroblasts of Patients With Graves Ophthalmopathy.

In the present study, the authors investigated the effects of selenium on inflammation, hyaluronan production, and oxidative stress in primary cultured orbital fibroblasts of patients with Graves ophthalmopathy (GO). Orbital adipose/connective tissue specimens were obtained during the course of orbital surgery for patients with GO (n = 7) and other noninflammatory problems (n = 5). After incubation with various concentrations of sodium selenite for 48 hours, supernatants from primary cultures were collected. Hyaluronan and cytokine levels were measured using commercially available enzyme-linked immunosorbent assay kits. To determine the effect of selenium on reactive oxygen species (ROS) production stimulated by H2O2 (100 μM) for 30 minutes, the cells were pretreated with various concentrations of sodium selenite for 60 minutes. Interleukin (IL)-6 and tumor necrosis factor-alpha levels were significantly higher in orbital fibroblasts of patients with GO than in orbital fibroblasts of control patients. Hyaluronan production was suppressed by selenium in cultured orbital fibroblasts of patients with GO. Inflammatory cytokines such as IL-1α, IL-8, and tumor necrosis factor-alpha were suppressed by selenium in cultured orbital fibroblasts of patients with GO. IL-1β and IL-6 were not suppressed by selenium in cultured orbital fibroblasts of patients with GO. Selenium pretreatment reduced intracellular ROS generation stimulated by H2O2 in cultured orbital fibroblasts of patients with GO. In conclusion, hyaluronan production, inflammatory cytokines, and intracellular ROS generation were suppressed by selenium in cultured orbital fibroblasts of patients with GO. Several inflammatory cytokines may be suppressed by selenium in cultured orbital fibroblasts of patients with GO. This study provide the basis for use of selenium in the treatment of GO.

Vitamin E and selenium treatment of monocrotaline induced hepatotoxicity in rats

Monocrotaline (MCT) is a hepatotoxic pyrrolizidine alkaloid that is derived from plants; exposure may occur by consumption of contaminated grains, herbal teas and medicines. MCT can cause liver damage. We investigated the antioxidant effects of selenium (Se) and vitamin E against the toxic effects of MCT. Female Wistar albino rats were divided into four groups: a control group, an MCT group, an MCT + Se group, and an MCT + vitamin E group. Liver tissues were harvested, fixed, processed to paraffin and sections were cut. Anti-von Willebrand factor (vWF) immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL), and hematoxylin and eosin staining were performed. Serum and liver tissue glutathione (GSH), catalase (CAT), and glutathione peroxidase (GPx) levels were measured. Histopathological and TUNEL data showed significantly increased liver damage in the MCT group compared to controls. Histopathological and TUNEL staining indicated significant improvements in the MCT + vitamin E and MCT + Se groups compared to the MCT group. MCT significantly reduced the serum GSH level and GPx activity, and liver GPx activity. Biochemical data indicated a significant improvement in serum GSH level in the MCT + vitamin E group compared to the MCT group. We suggest that vitamin E and Se afford limited protection against MCT hepatotoxicity.

Protecting Role of Selenium on the Cytotoxic Effect of Profenofos on Rabbit Fertility

Profenofos is an Organophosphorous compound and acaricide used in Egypt with cumulative toxic effects causing reproductive dysfunction and increase in reactive oxygen species production. Protective and anti-oxidant effects of selenium can improve the activity of radical scavenger. So, the aim of this study was to elucidate the protective effects of Selenium against reproductive toxicity induced by Profenofos in male and female New Zealand rabbits (n=18). Three experimental groups (3 males and 3 females per each group) receiving a combination of Profenofos (70 mg/ kg b. w.) and/or selenium in drinking water (25 mg/ kg b. w.) for 90-day was divided as follows: non treated (control), Profenofos alone and Profenofos + selenium group. Profenofos caused a decrease in body and organs weights compared to control group. It had a fetotoxic effect resulting in a significant reduction in pregnancy rate and the number of viable feti in treated animals. Also, Profenofos caused a significant elevation in ALT, AST, MDA, urea and creatinine, while a significant decrease was noticed in SOD, GSH, testosterone, estrogen and progesterone in all treated rabbits compared to control group. Concomitant administration of selenium with Profenofos alleviated the induced alterations. In addition to, histopathological results revealed that testes, epididymis, ovary and uterus alterations represented by degenerative and inflammatory changes as a result of Profenofos exposure. Profenofos had a carcinogenic effect on uterus as leiomyoma with rhabdomyosarcoma which gave positive immunoreactivity with Desmin and Smooth muscle actin. Also, Profenofos caused histopathological and histochemical effects in liver and kidney tissues. There was intensive positive immunoreactivity for caspase- 3 (dark brown granules) was observed in the cytoplasm of apoptotic testicular, ovarian and uterine cells that indicating the severity of Profenofos toxicity. On the other hand, examined tissues of Profenofos in combination with selenium treated group showed apparent reduction of caspase-3 immunoreactivity to be more or less similar to the control group. In conclusion, selenium is a valuable cytoprotective which reduced the oxidative stress toxicity induced by Profenofos in the reproductive system of male and female as well as liver and kidney albino rabbits.

Antioxidant effect of selenium and its Nano form on oxidative stress induced by iron overload

Antioxidant effect of selenium and its Nano form on oxidative stress induced by iron overload

Effect of Different Selenium Sources on Antioxidant Enzymes and Bioavailability in Goats

To assess the antioxidant effect of selenium (Se) yeast and sodium selenite, 18 non-descript male kids (2–3 months old, 6.63±0.24 kg body weight) were divided into three groups (6 each) following completely randomized design. Animals in the control group (T1) were fed concentrate mixture and oat straw ad libitum, while animals in T2 and T3 were additionally supplemented with 0.30 mg selenium/kg of diet through Se yeast and sodium selenite, respectively. RBC GSH-Px activity was significantly (P<0.05) higher in T2 and T3 as compared to T1. CAT activity of erythrocytes increased significantly (P<0.05) in T2 and T3 kids compared to control kids. Malonaldehyde (MDA) values were significantly (P<0.05) lower in T2 and T3 as compared to control. The SOD enzyme activity was significantly (P<0.05) higher in kids supplemented with organic Se compared to other groups The mean Se levels in serum of kid at 180 days of the experiment were 210, 330 and 265 ppb in T1, T2 and T3 groups, respectively. It was found that supplementation of selenium both in organic and inorganic form significantly (P<0.05) increased antioxidant enzymes activity and Se bioavailability in goats, organic Se was more effective than inorganic Se.

Antioxidant effects of selenium on lung injury in paraquat intoxicated rats

Context. Paraquat (PQ) causes lethal intoxication by inducing oxidant injury to the lung. Selenium is a cofactor for glutathione peroxidase (GPx), which is one of the major endogenous antioxidant enzymes. Objective. To determine whether selenium post-treatment activates GPx, decreases lung injury, and improves survival in PQ intoxicated rats. Materials and methods. Male Spraque–Dawley rats were categorized into three groups: sham (n = 6), PQ (n = 12), and PQ + Se (n = 12). In the PQ and PQ + Se groups, 50 mg/kg of PQ was administered intraperitoneally. After 10 minutes, 60 μg/kg of Se (PQ + Se) or saline (PQ) was administered via the tail vein. Six rats per group were euthanized 6 hours or 24 hours later. Lung tissues were harvested for the measurement of GPx activity, reduced glutathione (GSH), glutathione disulfide (GSSG) and malondialdehyde (MDA) and for histological analysis. Using separated set of rats, survival of PQ (n = 10) and PQ + Se (n = 10) were observed for 72 hours. Results. GPx activity in the PQ group at the 6-hour and 24-hour time points was lower than in the sham group (p < 0.006). GPx activity in the PQ + Se group at the 6-hour and 24-hour time points was higher than in the PQ group at the same time (p < 0.006). GPx activity in the PQ + Se group at 24 hours was higher than at 6-hour time point and also higher than in the sham group (p < 0.006). The GSH/GSSG ratio in the PQ + Se group at 24 hours was lower than that in the sham group (p < 0.006). MDA levels in the PQ group at 6 hours and 24 hours were higher than in the sham group (p < 0.006). MDA levels at 24 hours in the PQ + Se group was lower than in the PQ group (p < 0.006). Acute lung injury (ALI) scores in the PQ group at 6 hours and 24 hours were higher than in the sham group (p < 0.006). ALI scores at 24 hours in the PQ + Se group were lower than in the PQ group. Survival rates did not differ between PQ and PQ + Se (p = 0.869). Conclusion. Single dose of selenium post-treatment activates GPx and attenuates lipid peroxidation and lung injury early after paraquat intoxication, but does not improve 72 hours of survival.

Efeitos antioxidantes do selênio e seu elo com a inflamação e síndrome metabólica

O estado inflamatório crônico e de baixo grau bem como o estresse oxidativo associados à síndrome metabólica são fatores de risco relevantes para o desenvolvimento de doenças cardiovasculares. Neste contexto, o selênio é um mineral essencial que se encontra associado com o correto funcionamento dos principais processos metabólicos celulares. Estudos in vitro e in vivo em modelos experimentais de síndrome metabólica, bem como em humanos, tem investigado o efeito do selênio sobre a expressão e secreção de biomarcadores de inflamação e de estresse oxidativo. Para obtenção dos artigos sobre efeitos antioxidantes do selênio foram feitas pesquisas nos websites científicos. Na literatura encontramos numerosos artigos sobre os diferentes parâmetros modulados pelas concentrações plasmáticas de selênio, incluindo a proteína-C reativa, a interleucina-6, o fator de necrose tumoral-α, a interleucina-1β e a proteína transportadora de retinol-4. Esta revisão teve por objetivo discutir o papel do selênio nos processos inflamatórios e de estresse oxidativo, associados à síndrome metabólica.

Abstract 5664: Methylseleninic acid induces NAD(P)H: quinone oxidoreductase-1 expression through activation of NF-E2-related factor 2 in Chang liver cells

Abstract Selenium, an essential biological trace element, has been shown to reduce the incidence of cancer and to inhibit the experimentally induced tumorigenesis. Selenium has been reported to induce expression of some antioxidant enzymes in various cell lines. However, the mechanisms underlying its chemopreventive as well as antioxidant effects of selenium remain largely unresolved. In the present study, we found that methylseleninic acid (MSeA), a monomethylated selenium compound, induced expression of NAD(P)H-quinone oxidoreductase-1 (NQO-1) in Chang human liver cells. NQO-1 is an important antioxidant enzyme that plays a pivotal role in cytoprotection against oxidative and electrophilic stresses. NF-E2-related factor 2 (Nrf2), through interaction with antioxidant response element (ARE), upregulates expression of several phase-2 detoxifying and antioxidant enzymes including NQO-1. MSeA treatment (3 μM) resulted in an increased nuclear translocation, subsequent ARE binding and transactivation of Nrf2. Silencing Nrf2 using dominant negative Nrf2 or Nrf2 siRNA markedly reduced the MSeA-induced NQO-1 expression. The binding of Nrf2 to ARE was verified by the chromatin immunoprecipitation (ChIP) assay. We also found that MSeA treatment induced expression of NQO-1 to a much lesser extent in Nrf2 knock out (−/−) mouse embryonic fibroblast (MEF) than in Nrf2 wild-type (+/+) MEF. One of the critical events responsible for Nrf2 activation is its dissociation from the repressor protein Keap1. MSeA reduced the level of Keap1 protein at a post-translational level. Moreover, ubiquitination of Keap1 was markedly increased in cells exposed to MSeA, which resulted in decreased steady-state levels of Keap1 in parallel with inhibition of keap1-dependent ubiquitination of Nrf2. siRNA knock-down of Keap1 significantly increased both constitutive and MSeA-induced NQO-1 expression. We hypothesize that MSeA may modify Keap1 thiols, which facilitates the nuclear translocation and ARE binding of Nrf2. In addition, prior exposure of cells to dithiothreitol (1 mM) blocked NQO-1 induction by MSeA, corroborating Keap1 thiol modification involved in Nrf2 activation. Oral administration of MSeA (1 mg/kg) by gavage to mice also induced NQO-1 protein expression in the liver. Methylselenol generated from selenomethionine (SeMet) by methioninase (METase) activity induced expression of NQO-1. In contrast to SeMet formed by METase, SeMet failed to induce NQO-1 expression, suggesting that methylselenol, not its metabolite, is directly responsible for NQO-1 induction. Taken together, these results suggest that MSeA, the immediate precursor of methylselenol, upregulates the expression of NQO-1 via the Keap1-Nrf2 signaling, preferentially by targeting cysteine thiol(s) present in Keap1. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5664.

Antioxidant Effects of Selenium in Rat Brain and the Stimulating Role of Nitric Oxide

Objective: To evaluate the antioxidant effect of selenium on Na<PRE>+</PRE>, K<PRE>+</PRE>-ATPase in rat brain in the presence of nitric oxide.Methods: Male Wistar rats (70 g) were treated as follows: group 1 received 1 μg of i.p. sodium nitroprusside per kg (SNP), group 2 received 5 μg sodium selenite during 20 days, group 3 received sodium selenite 5 μg+SNP 1 μg and the control group received vehicle 50 μl (0.9% NaCl), same period and route. At the end of treatment, animals were sacrificed and their brain dissected into cortex, hemispheres, cerebellum and brain stem in order to determine lipid peroxidation (TBARS), Na<PRE>+</PRE>, K<PRE>+</PRE> ATPase and total ATPase in each section. Blood hemoglobin concentration (Hb) and prostate weight were also assessed.Results: A significant increase of Hb in blood and of proteins in cortex and hemisphere was detected, but TBARS values fell due to the effect of sodium selenite in all examined regions, except for cerebellum. ATPase activity declined in all groups and regions with and without NTP. We conclude that diet supplementary selenium to inhibit NO generation can be a useful treatment in chronic inflammatory diseases.

Role of selenium in reducing hypoxia-induced oxidative stress: an in vivo study

At high altitudes, the reactive oxygen species are continuously generated as a consequence of low oxygen partial pressure (hypoxia), which causes tissue damage. The body’s defence system to combat the oxidative stress (e.g., anti-oxidant enzymes, free radical scavengers such as vitamin C, vitamin E, β-carotene, reduced glutathione and minerals such as selenium, etc.) may diminish. In the present study, the antioxidant effect of selenium (Se) in reducing the hypoxia-induced oxidative stress was evaluated by exposing male albino rats to hypoxic stress in a decompression chamber. Exposure to hypoxia resulted in an increase in malondialdehyde (MDA) levels in plasma and tissues and a concurrent decrease in blood glutathione (GSH), glutathione peroxidase (GPx), plasma protein and plasma selenium content when compared with controls. Haemoglobin concentration (Hb%), red blood corpuscles (RBC) and white blood corpuscles (WBC) count were also increased in the hypoxia-exposed group. Selenium supplementation to animals reversed the trend. There was a significant decrease ( P < 0.001) in MDA and subsequent increase in plasma and tissue GSH levels. Similarly the blood and tissue GPx and plasma protein also increased significantly in the Se supplemented animals compared with control animals. The Hb%, RBC and WBC counts showed no significant difference between Se-fed and control rats. These results suggest that selenium may help in reducing the lipid peroxidation during hypoxia.