Effect Of Sodium Selenite Research Articles

Protective effects of sodium selenite and selenium nanoparticles against experimental colon carcinogenesis in mice

Protective effects of sodium selenite and selenium nanoparticles against experimental colon carcinogenesis in mice

Sodium Selenite Protects Against Silver Nanoparticle-Induced Testicular Toxicity and Inflammation.

Metal nanomaterials hold great potential and play an important role in consumer products. However, the increasing use of nanomaterials has raised concern over inadvertent exposure and potential risks for human health and the environment. Henceforth, in vivo testing of nanoparticles and protection against its toxicity is required. Using rat as an animal model, effect of sodium selenite (Se), an essential trace element, on rat testes exposed to silver nanoparticles (AgNPs) was evaluated. Male rats were treated with AgNPs (5mg/kg/b.w) i/p or Se (0.2mg/kg/b.w) by gavage. AgNP administration decreased Glutathione (GSH) levels and activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and increased levels of malondialdehyde (MDA) and expression of interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α). However, treatment with Se increased GSH levels and activities of SOD, CAT, and GPx compared with AgNP-treated group and decreased the level of MDA and inflammatory biomarkers significantly (p<0.05) as compared with AgNP-treated group. Light microscopic analyses also revealed that AgNP induced histopathological changes in testes tissue. Further, protection by Se on biochemical results was confirmed by alleviation of the histopathological changes in the tissue. Results show the adverse effects of AgNPs on the male reproductive tract, particularly spermatogenesis, and suggest that Se possesses significant potential in reducing AgNP-induced testicular toxicity.

Sodium Selenite Inhibits Proliferation of Gastric Cancer Cells by Inducing SBP1 Expression.

Selenium is an essential trace element with an inhibitory effect on many types of human cancers, including gastric cancer. Selenium-binding protein 1 (SBP1) has been shown as a possible mediator of selenium's anti-cancer functions. Indeed, SBP1 was downregulated in gastric cancer, which is related with poor prognosis. However, the molecular mechanisms underlying the anti-tumor effects of SBP1 remain poorly understood. In this study, we aimed to assess the effects of selenium and/or SBP1 on the proliferation of gastric cancer cells. We used SGC7901 and N87 human gastric cancer cell lines and nude mice carrying subcutaneously implanted SGC7901 cells. Treatment with sodium selenite for 48 h caused the inhibition of cell proliferation and the increase in apoptosis of SGC7901 and N87 cells. Furthermore, sodium selenite increased the expression level of SBP1 and decreased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and the Wnt pathway components and its downstream targets, including β-catenin, GSK-3β, c-myc and cyclinD1 in these cell lines. However, these effects of sodium selenite were attenuated in SGC7901 and N87 cells by knockdown of SBP1 expression. Thus, the sodium selenite-induced SBP1 expression is associated with the inhibition of cell proliferation and with the induced apoptosis. Importantly, sodium selenite treatment retarded the growth of the transplanted SGC7901 cells in nude mice, with the induction of SBP1 expression, which was associated with the decrease of Nrf2 expression and the inactivation of the Wnt/β-catenin signaling pathway. We suggest that sodium selenite may have a potential application in gastric cancer treatment.

Effect of Sodium Selenite on Pathological Changes and Renal Functions in Broilers Fed a Diet Containing Aflatoxin B₁.

To evaluate the renal toxicity of dietary aflatoxin B1 (AFB1) and ameliorating effects of added dietary sodium selenite in broiler, renal histopathological changes, ultrastructural changes, and renal function parameters were monitored at 7, 14, and 21 days of age. Two hundred one-day-old healthy male Avian broilers were divided into four groups, namely control group, AFB1 group (0.3 mg/kg AFB1), +Se group (0.4 mg/kg Se), and AFB1+Se group (0.3 mg/kg AFB1+0.4 mg/kg Se). Compared with that of the control group, the relative weight of kidney was increased in the AFB1 group. There were no significant differences between the AFB1+Se group and the control group. By histopathological observation, the renal epithelia were swelling and necrosis at 7 and 21 days of age. Ultrastructurally, the lipid droplets and expanded endoplasmic reticulum appeared in the plasma of epithelia cells in the AFB1 group. Enlarged mitochondria with degenerated cristae were observed in the +Se group. Compared with the control group, the contents of serum creatinine and serum uric acid in the AFB1 group were increased, while the activity of renal Na+-K+ ATPase was decreased. When 0.4 mg/kg selenium was added into the diet containing 0.3 mg/kg AFB1, there were no obvious histological changes in the AFB1+Se group, and the contents of the serum creatinine and serum uric acid contents and the activity of renal Na+-K+ ATPase were close to those in the control group. In conclusion, sodium selenite exhibited protective effects on AFB1-induced kidney toxicity in broilers.

The Effects of Lead and Selenium on Melanoma Induction

Background: Melanoma is a malignant skin cancer and is one of the most aggressive malignancies in humans. Heavy metals, including lead, are known to cause cellular toxicity and have been studied for their potentials to induce apoptosis in tumor cells. Since selenium is considered to act protectively in cases of lead poisoning, this study focused on the effects of sodium selenite and lead chloride, both alone and combined, on melanoma cell apoptosis. Methods: This study was carried out by doing cell culture of melanoma cells (B16-F10 cell line) and using C57BL/6 mice. Melanoma cells suspended in lead (II) chloride, sodium selenite, or lead (II) chloride + sodium selenite solutions were injected subcutaneously to mice to induce tumor growth. After 12 days, tumors were excised and measured, followed by flow cytometry and a statistical analysis using a one-way ANOVA. Results: In the group of mice receiving a single injection of melanoma cells suspended in 10 μmol/l of lead (II) chloride, the growth of tumor was significantly slower than in the control group. In mice treated with lead (II) chloride 50 μmol/l and 100 μmol/l, no tumor was visible at the end of the experiment. With a single injection of lead (II) chloride and sodium selenite at concentrations ≥ 10 μmol/l, the weight and size of the tumor were substantially smaller than in the control group. Conclusion: The effect of lead (II) chloride on melanoma induction is dependent on the concentration of lead (II) chloride. Future applications may include the use of lead (II) chloride to increase apoptosis and necrosis in tumor cells and thus suppress tumor cells proliferation.

Effect of Sodium Selenite on Lipid Peroxidation and Glutathione in Alloxan Induced Diabetic Rats

Background: Diabetes-related dysfunctions are the major causes of mortality and morbidity for diabetic patients. Objectives: Selenium is a potent antioxidant. In the present study, we examined antioxidative activities of sodium selenite and possible protective effect of it on serum, liver and kidney lipid peroxidation and glutathione in alloxan-induced type 1 diabetic rats. Materials and Methods: In this experimental study 40 Sprage Dawley male rats were divided into 4 groups randomly; group I as control, group II as sham treated with sodium selenite (1 mg/kg i.p. daily), group III as diabetic untreated, and group IV as diabetic treated with sodium selenite (1 mg/kg i.p. daily) after induce diabetes, respectively. Diabetes was induced in the 3rd and 4th groups by alloxan injection (s.c.). After 8 weeks, animals were anaesthetized, liver and kidney were then removed immediately and used fresh or kept frozen until analysis. Blood samples were also collected before killing of the rats to measure the lipid peroxidation and glutathione level. Results: Liver and kidney content of lipid peroxidation decreased in diabetic treated group compared with untreated group. Kidney content of glutathione significantly increased in diabetic treated group compared with untreated group. Serum level of glutathione and liver content of it slightly increased in diabetic treated group compared with untreated group. Conclusions: This study showed that sodium selenite might be a potent antioxidant and exert beneficial effects on the lipid peroxidation and glutathione in alloxan-induced type 1 diabetic rats.

Effect of Sodium Selenite on Lipid Peroxidation and Glutathione in Alloxan Induced Diabetic Rats

Effect of Sodium Selenite on Lipid Peroxidation and Glutathione in Alloxan Induced Diabetic Rats

Effect of Sodium Selenite on Lipid Peroxidation and Glutathione in Alloxan Induced Diabetic Rats

Background:: Diabetes-related dysfunctions are the major causes of mortality and morbidity for diabetic patients. Selenium is a potent antioxidant. In the present study, we examined antioxidative activities of sodium selenite and possible protective effect of it on serum, liver and kidney lipid peroxidation and glutathione in alloxan-induced type 1 diabetic rats. Materials and Methods:: In this experimental study 40 Sprage Dawley male rats were divided into 4 groups randomly; group I as control, group II as sham treated with sodium selenite (1 mg/kg i.p. daily), group III as diabetic untreated, and group IV as diabetic treated with sodium selenite (1 mg/kg i.p. daily) after induce diabetes, respectively. Diabetes was induced in the 3rd and 4th groups by alloxan injection (s.c.). After 8 weeks, animals were anaesthetized, liver and kidney were then removed immediately and used fresh or kept frozen until analysis. Blood samples were also collected before killing of the rats to measure the lipid peroxidation and glutathione level. Results:: Liver and kidney content of lipid peroxidation decreased in diabetic treated group compared with untreated group. Kidney content of glutathione significantly increased in diabetic treated group compared with untreated group. Serum level of glutathione and liver content of it slightly increased in diabetic treated group compared with untreated group. Conclusions:: This study showed that sodium selenite might be a potent antioxidant and exert beneficial effects on the lipid peroxidation and glutathione in alloxan-induced type 1 diabetic rats.

Protective effects of sodium selenite against aflatoxin B1on haemoglobin content, erythrocyte count, and immune adherence function in broilers

Aflatoxin B1 (AFB1), commonly found in feed stuffs causes hepatocellular carcinoma and immunosuppression. Selenium (Se) is mainly known as an important antioxidant and immunostimulant. To evaluate the protective effects of dietary sodium selenite against AFB1_induced erythocytic toxicology, one hundred male Avian broilers were randomly divided into five groups viz. : fed with basal diet (control group), 0.3mg/kg AFB1 (AFB1 group), 0.3mg/kg AFB1+0.2mg/kg Se (+Se group ‘!), 0.3mg/kg AFB1+0.4mg/kg Se (+Se group a!) and 0.3mg/kg AFB1+0.6mg/kg Se (+Se group b!), respectively. At 7, 14 and 21 days of the experiment, the red blood cells (RBC count), content of hemoglobin (Hb) and the immune adherence function were determined. Compared with control group, the number of RBC in AFB1 group was increased, while the content of Hb and erythrocyte rosette rates in AFB1 group were decreased significantly. Dietary sodium selenite, however, could decrease the number of RBC; increase the content of Hb and erythrocyte rosette rate significantly. It was indicated that sodium selenite in the diets could exert protective effects against AFB1-induced damage on the red blood cells, and the transport capacity and immune adherence function of erythocyte could be maintained.

Effect of sodium selenite on chosen anti- and pro-oxidative parameters in rats treated with lithium: A pilot study

BackgroundSelenium is an essential element of antioxidant properties. Lithium is widely used in medicine but its administration can cause numerous side effects including oxidative stress. The present study aimed at evaluating if sodium selenite could influence chosen anti- and pro-oxidant parameters in rats treated with lithium. MethodsThe experiment was performed on four groups of Wistar rats: I (control) – treated with saline; II (Li) – treated with lithium (2.7mgLi/kg b.w. as Li2CO3), III (Se) – treated with selenium (0.5mgSe/kg b.w. as Na2SeO3), IV (Li+Se) – treated with Li2CO3 and Na2SeO3 together at the same doses as in group II and III, respectively. All treatments were performed by stomach tube for three weeks in form of water solutions. The following anti- and pro-oxidant parameters: total antioxidant status (TAS) value, catalase (CAT) activity, concentrations of ascorbic acid (AA) and malonyldialdehyde (MDA) in plasma as well as whole blood superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured. ResultsSelenium given alone markedly enhanced whole blood GPx and diminished plasma CAT vs. control. Lithium significantly decreased plasma CAT and slightly increased AA vs. control. Selenium co-administration restored these parameters to the values observed in control animals. Furthermore, selenium co-administration significantly increased GPx in Li-treated rats. All other parameters (TAS, SOD and MDA) were not affected by lithium and/or selenium. ConclusionFurther research seems to be warranted to decide if application of selenium as an adjuvant in lithium therapy is worth considering.

Six-day selenium supplementation led to either UVA-photoprotection or toxic effects in human fibroblasts depending on the chemical form and dose of Se.

Selenium (Se) is an essential trace element with a narrow safety zone and unclear effects on skin photoageing. The aim of this work was to investigate the photoageing properties of sodium selenite or selenomethionine (SeMet) after a long term (6 days) Se supplementation in normal human skin fibroblasts (NHSF) subjected to ultraviolet-A (UVA) irradiation inducing 30% cell death. The uptake, toxicity and antioxidant effects of sodium selenite and SeMet were compared to better understand their photoageing properties. SeMet uptake was better than sodium selenite and their uptake by fibroblasts was not via an actively transport process. Sodium selenite induced a higher toxicity than SeMet. At 5 μM, sodium selenite inhibited cell proliferation associated with a blockage in the G2 phase and induced DNA fragmentation leading to caspase-3-dependent apoptosis cell death. At low doses (<1 μM), SeMet and sodium selenite induced glutathione peroxidase-1 (GPX1) activity and selenoproteinW1 (SEPW1) transcript expression but metalloproteinase (MMP)-1 was only induced by sodium selenite. SeMet and sodium selenite did not protect NHSFs from UVA-induced cell death. However, SeMet decreased malondialdehyde (MDA) and protected NHSFs from UVA-induced MMP1 and MMP3. We then observed a large difference in terms of photoprotection according to selenium forms. SeMet may be a potential agent for the prevention and treatment of skin photoageing.

Effect of injectable sodium selenite on the level of stress biomarkers in male aardi goats

The aim of the present study was to evaluate the effects of sodium selenite (SS) injection on plasma concentrations of selenium (Se), glutathione peroxidase (GSH-Px); Malondialdehyde (MDA), and cortisol. A total of twenty seven male Aardi goats were randomly divided into three equal groups; group I (control, fed selenium deficient diet), II (injected with 0.01 mg SS/kg body weight) and III (injected with 0.05 mg SS/kg body weight). Plasma selenium levels differed significantly between treatment and control groups from week one to week three. Level of GSH-Px also differed significantly between the groups. Cortisol varied according to selenium supplementation in week one, two and three. Sodium selenite injection significantly increased Se levels in plasma of Aardi goats as compared with the control group. In conclusion, sodium selenite treatment to Aardi goats minimized the stress level in male Aardi goats, and it was difficult from the experimental design to recommend one of the two doses as therapeutic or preventive anti stress protocols.

Effect of Sodium Selenite on Testicular Damage Induced by Cisplatin in Adult Male Rats

Cisplatin is an established chemotherapeutic substance commonly used in the treatment of cancer. Several reports have been published on its antineoplastic activity and toxicity however, no details are available on its noxious effects on the genital system organs such as testes. Another interesting element Selenium and its derivatives including Sodium selenite are reported to form the active center of glutation peroxidase which has antioxidant properties involved in antioxidant balance of the cells and in lipid peroxidation. This study was aimed to explore the effects of selenium against the damage caused in testes of rats by Cisplatin treatment. Sprague-Dawley rats 28 in number were randomly allotted to different standard and treatment groups. All the animals in different experimental groups were maintained under controlled standard conditions. The results clearly demonstrated that Cisplatin treatment decreased the weight of testes as well as the body weight of rats. Furthermore, it damaged seminiferous tubules and cells in testes of animals in the treatment groups, and halted the process of spermatogenesis. Selenium treatment reduced the damage caused by Cisplatin treatment. The results of the present study were substantiated by detailed histopathological investigations

Effects of sodium selenite and chromium sulphate as metabolic modifiers on stress alleviation, performance and liver mineral contents of feedlot Bonsmara cross steers

The objective of the study was to investigate the effects of supplemental selenium and chromium on blood cortisol and glucose levels on stress alleviation and the carry-over effects on performance and liver mineral contents of local beef cattle under feedlot conditions. Seventy-two Bonsmara cross weaned calves weighing on average 185 ± 20.729 kg were allocated to 12 pens of six animals each, three replicates per treatment and fed for 120 days either a standard diet (CON) or supplemented with 0.3 mg.kg –1 DM sodium selenite (SEL) 0.3 mg.kg –1 DM chromium sulphate (CHR) and a combination of Se and Cr (SEL/CHR). Blood cortisol and glucose levels as stress parameters, feed intake and growth performance parameters were assessed. There was no statistical difference in blood cortisol levels on d0. On d14, cortisol concentrations were lower than on d0 (P<0.05) except for treatment SEL/CHR. On d42, the values were higher than on d0 and d14 except for SEL/CHR that had very low cortisol values (P<0.05). Blood glucose concentrations followed similar trend. There was no carry-over effect of stress alleviation on growth performance though SEL/CHR tended to have better ADG (P=0,148) and predicted FCR (P=0,197). Liver tissue mineral levels were within normal ranges. However, SEL increased significantly (P<0.05) liver Ca, Mg, Co and Mn while CHR decreased Ca and Mg concentrations. Selenium was positively correlated with Cu (r=0.30, P= 0.01) and phosphorus (r=0.44, P=0.0001) while Cr was negatively correlated with Ca (r=-0.50, P=0.01) and Mg (r=-0.30, P=0.01). Liver tissue minerals did not affect performance parameters. SEL/CHR might act better on stress alleviation and growth improvement. The effects on carcass characteristics and meat quality and the use of different forms of supplemental Se and Cr warrant further research. Key words: Selenium, chromium, stress, cortisol, glucose, feedlot, Bonsmara.

Effects of sodium selenite on the decreased percentage of T cell subsets, contents of serum IL-2 and IFN-γ induced by aflatoxin B1 in broilers

Aflatoxin B1 (AFB1), especially inducing hepatocellular carcinoma and immunosuppression of animals, poses a serious healthy and economic hazard to both humans and livestock. Animal studies have demonstrated that selenium (Se) provides anticarcinogenic and antimutagenic effects against AFB1. However, the effects of Se against AFB1-induced immunosuppression were rarely reported. To test this, three hundred 1-day-old male avian broilers were divided into five groups and fed on control diet (0.4mg/kg Se), AFB1 group(0.3mg/kg AFB1+0.4mg/kg Se), AFB1+Se group I(0.3mg/kg AFB1+0.6mg/kg Se), AFB1+Se group II(0.3mg/kg AFB1+0.8mg/kg Se) and AFB1+Se group III(0.3mg/kg AFB1+1.0mg/kg Se) for 21days (n=60/group). Although the body weight in AFB1 group was lower than that in control group at 14days of age, there no significant differences on body weight among five groups at 7 and 21days of age. No evident clinical symptoms were observed among five groups from 7 to 21days of age. The percentages of peripheral blood CD3+, CD3+CD4+, CD3+CD8+ and the contents of serum IL-2 and IFN-γ in AFB1 group were decreased, compared with those in control group. Compared with those in AFB1 group, the percentages of CD3+, CD3+CD4+ and CD3+CD8+ T cells in three AFB1+Se groups were increased from 14 to 21days of age, and the contents of serum IL-2 and IFN-γ in all AFB1+Se groups were increased from 7 to 21days of age. On the contrary, the percentages of CD3+, CD3+CD4+ and CD3+CD8+ T cells, and the contents of Serum IL-2 and IFN-γ in AFB1+Se group III were lower than those in AFB1+Se group II. It was concluded that 0.6 and 0.8mg/kg Se could increase the decreased percentages of peripheral blood T-cell subsets and the contents of serum IL-2 and IFN-γ induced by 0.3mg/kg AFB1 in the diets, and cellular immune function could be improved in chickens.

The effect of sodium selenite on lead induced cognitive dysfunction

The effect of lead (Pb) on spatial memory and hippocampal long-term potentiation (LTP) as a key risk factor has been widely recognized and the oxidative damage has been proposed as a possible mechanism of lead neurotoxicity. Selenium (Se) is a nutritionally essential trace element with known antioxidant potential. In this study we investigated the effect and the underlying mechanisms of Se supplementary on Pb induced cognition and synaptic plasticity impairment. Lactating Sprague-Dawley rats (SD rats) were randomly divided to four groups: 0ppm lead acetate (Pb); 0ppm Pb and 0.2ppm sodium selenite (Se); 100ppm Pb; 100ppm Pb and 0.2ppm Se. Lactating rats were treated with or without Pb and/or Se throughout lactation until weaning. The levels of hippocampal LTP, the spatial memory, the apoptosis of hippocampal neurons, the levels of lactate dehydrogenase (LDH) release, and the serum level of superoxide dismutase (SOD) and malondialdehyde (MDA) were assayed. It had been observed that in Pb group the spatial memory, the induce level of LTP, the serum SOD level decreased, the LDH release level, the neurons apoptosis level, the serum MDA level increased, while in the Se supplements groups, the spatial memory, the induce level of LTP increased significantly. Compared with the Pb group, Se supplements shown down regulated the level of LDH, the neurons apoptosis and the serum MDA, and up regulated the level of serum SOD. We could draw the conclusion that Se supplements could alleviate toxic effect of lead on hippocampal LTP and spatial memory. The treated with selenium around 0.2ppm may protect against spatial memory dysfunction induced by lead exposure.

Selenium Protects Bone Marrow Stromal Cells Against Hydrogen Peroxide-Induced Inhibition of Osteoblastic Differentiation by Suppressing Oxidative Stress and ERK Signaling Pathway

Osteoporosis is a bone disease that leads to an increased risk of fracture. Oxidative stress may play a major role in the development of osteoporosis in part by inhibiting osteoblastic differentiation of bone marrow stromal cells (MSCs). Some evidence suggested that antioxidant selenium could prevent osteoporosis, but the underlying mechanism remains unclear. In this work, the effect of sodium selenite on H₂O₂-induced inhibition of osteoblastic differentiation of primary rat bone MSCs and the related mechanisms were examined. Pretreatment with selenite inhibited the adverse effect of H₂O₂ on osteoblastic differentiation of MSCs, based on alkaline phosphatase activity, gene expression of type I collagen and osteocalcin, and matrix mineralization. In addition, selenite pretreatment also suppressed the activation of extracellular signal-regulated kinase (ERK) induced by H₂O₂. The above effects were mediated by the antioxidant effect of selenite. Selenite enhanced the gene expression and activity of glutathione peroxidase, reversed the decreased total antioxidant capacity and reduced glutathione, and suppressed reactive oxygen species production and lipid peroxidation level in H₂O₂-treated MSCs. These results showed that selenite protected MSCs against H₂O₂-induced inhibition of osteoblastic differentiation through inhibiting oxidative stress and ERK activation, which provided, for the first time, the mechanistic explanation for the negative association of selenium status and risk of osteoporosis in terms of bone formation.

Effects of Dietary Sodium Selenite and Selenium Yeast on Antioxidant Enzyme Activities and Oxidative Stability of Chicken Breast Meat

The effects of sodium selenite (SS) and selenium yeast (SY) alone and in combination (MS) on the selenium (Se) content, antioxidant enzyme activities (AEA), total antioxidant capacity (TAC), and oxidative stability of chicken breast meat were investigated. The results showed that the highest (p < 0.05) glutathione peroxidase (GSH-Px) activity was found in the SS-supplemented chicken breast meat; however, SY and MS treatments significantly increased (p < 0.05) the Se content and the activities of catalase (CAT), total superoxide dismutase (T-SOD), and TAC, but decreased (p < 0.05) the malondialdehyde (MDA) content at 42 days of age. Twelve days of storage at 4 °C decreased (p < 0.05) the activity of the GSH-Px, but CAT, T-SOD, and TAC remained stable. SY decreased the lipid oxidation more effectively in chicken breast meat. It was concluded that SY and MS are more effective than SS in increasing the AEA, TAC, and oxidative stability of chicken breast meat.

Effect of sodium selenite on some enzymes of coelomic fluid to the immune response of holothurianApostichopus japonicus

The aquaculture of the sea cucumber Apostichopus japonicus(Echinodermata,Holothuroidea)has been growing rapidly over recent years in China in response to increasing consumer demand.Indeed,it has become an important sector of the marine industry in Northern China.However,with rapid growth and the use of non-standard practices and culture techniques,epidemic diseases of A.japonicus now pose increasing problems to the industry.Therefore,the healthy aquaculture of A.japonicus is important.For a reasonable evaluation of selenium effect on sea cucumber aquaculture,using laboratory tests to simulate the sodium selenite treatment and virus infection conditions,the detection and observation of the sea cucumber body cavity fluid immune enzyme changes,pathological changes and the relative rate of protection were made.The results showed that:the change of immune enzymes in coelomic fluid of sea cucumbers under simulated sodium selenite treatments and bacteria infected conditions was tested in order to reasonably evaluate the influence of selenium on aquaculture diseases.Results indicated that the activities of superoxide dismutase(SOD),glutathione peroxidase(GPx),lysozyme(LYZ),phenoloxidase(PO)and alkaline phosphatase(ALP)in coelomic fluid rose after sodium selenite treatments were enhanced.However,SOD,GPX and LYZ activities first ascended and then declined,and PO and ALP activities showed continued rise under additional pathogen injection into sea cucumbers,but the increasing extent of ALP activity was reduced along with increased sodium selenite concentration,and total diseased incidence rose and relative percent survival decreased under the severe sodium selenite treatment.This suggested that applying sodium selenite with moderate concentration could enhance immunity of sea cucumber to bacterial infection,but infecting also aggravated immune damage of sea cucumber by sodium selenite stress.Therefore,the diseases of cultured sea cucumber can be alleviated by optimized use of selenium.

The effect of sodium selenite on liver growth and thioredoxin reductase expression in regenerative and neoplastic liver cell proliferation

Selenium in supra-nutritional doses is tumour-preventative in animal models and in humans. In this work, we have compared the effect of sodium selenite on tumour growth in a rat hepatocarcinogenesis model with the effect of sodium selenite on the regeneration of liver mass after partial hepatectomy. In the tumour model, 5 μg/mL sodium selenite in the drinking water reduced the rate of tumour growth for up to 12 months after initiation; the volume fraction of liver cancers was 14 ± 4% with a mean bromodeoxyuridine-index of 19 ± 11% in the treated rats compared to a volume fraction of 26 ± 7% with a mean bromodeoxyuridine-index of 42 ± 27% in the control rats. Despite its efficacy in reducing tumour growth, 5 μg/mL sodium selenite treatment did not affect the gain of liver mass or the rate of cell proliferation after partial hepatectomy. In the regenerating livers, the activity of the cytosolic selenoenzyme thioredoxin reductase (TrxR1) was briefly and transiently increased, an increase further potentiated by sodium selenite. TrxR1 was selectively over expressed in proliferating liver tumours in relation to the surrounding liver tissue in the tumour model, as shown using immunohistochemistry analyses. We suggest that sodium selenite is a suitable candidate for liver cancer prevention in patients with chronic liver diseases that are dependent on sustained liver regeneration due to its differential effects on neoplastic and regenerative cell proliferation. Furthermore, the over expression of TrxR1 in liver neoplasia can only partly be explained by increased growth.