Protective Effect Of Sodium Selenite Research Articles

Detoxification of Selenium Yeast on Mycotoxins and Heavy Metals: a Review.

Mycotoxins are secondary metabolites produced by specific fungi. More than 400 different mycotoxins are known in the world, and the concentration of these toxins in food and feed often exceeds the acceptable limit, thus causing serious harm to animals and human body. At the same time, modern industrial agriculture will also bring a lot of environmental pollution in the development process, including the increase of heavy metal content, and often the clinical symptoms of low/medium level chronic heavy metal poisoning are not obvious, thus delaying the best treatment opportunity. However, the traditional ways of detoxification cannot completely eliminate the adverse effects of these toxins on the body, and sometimes bring some side effects, so it is essential to find a new type of safe antidote. Trace element selenium is among the essential mineral nutrient elements of human and animal bodies, which can effectively remove excessive free radicals and reactive oxygen species in the body, and has the effects of antioxidant, resisting stress, and improving body immunity. Selenium is common in nature in inorganic selenium and organic selenium. In previous studies, it was found that the use of inorganic selenium (sodium selenite) can play a certain protective role against mycotoxins and heavy metal poisoning. However, while it plays the role of antioxidant, it will also have adverse effects on the body. Therefore, it was found in the latest study that selenium yeast could not only replace the protective effect of sodium selenite on mycotoxins and heavy metal poisoning, but also improve the immunity of the body. Selenium yeast is an organic selenium source with high activity and low toxicity, which is produced by selenium relying on the cell protein structure of growing yeast. It not only has high absorption rate, but also can be stored in the body after meeting the physiological needs of the body for selenium, so as to avoid selenium deficiency again in the short term. However, few of these studies can clearly reveal the protective mechanism of yeast selenium. In this paper, the detoxification mechanism of selenium yeast on mycotoxins and heavy metal poisoning was reviewed, which provided some theoretical support for further understanding of the biological function of selenium yeast and its replacement for inorganic selenium. The conclusions suggest that selenium yeast can effectively alleviate the oxidative damage by regulating different signaling pathways, improving the activity of antioxidant enzymes, reversing the content of inflammatory factors, regulating the protein expression of apoptosis-related genes, and reducing the accumulation of mycotoxins and heavy metals in the body.

The use of selenium for protective and stimulating effects on plants when soil is contaminated with cadmium.

At the present time one of the tasks of modern agricultural industry consists in obtaining the ecologically safe and clean products. Contamination of soils with heavy metals due to an anthropogenic impact drives up their content in the composition of plant products. This shapes not only a reduction in crop yields, but also a deterioration in products quality. Within the terms of vegetation research in soil culture, there has been studied the protective and stimulating effect of sodium selenite upon the adaptive capacity of spring wheat plants of the variety Zlata under conditions of oxidative stress due to the soil contamination with cadmium. There has been studied the effect of different methods of sodium selenite application on the yield of spring wheat and the plants photosynthetic activity, depending on the level of soil contamination with cadmium. The object of research was a spring wheat variety Zlata. Plants have been cultivated in a greenhouse trial under soil culture conditions in Mitscherlich-vessels with a capacity of 6 kg of soil. Sod-podzolic soil has been used for research. Sodium selenite was introduced in three ways: pre-sowing seed treatment, foliar treatment of vegetative plants at the beginning of stage VI of organogenesis - the end of the tillering phase - the beginning of the stem-extension phase and the application of a salt solution into the soil when packing the vessels. The control samples represented variants without sodium selenite. To assess the plants photosynthetic productivity, there has been determined the chlorophyll content in plant leaves. The research results made it possible to determine the protective effect of sodium selenite on the adaptive capacity of plants under conditions of oxidative stress due to the soil contamination with cadmium. The increase in the adaptive capacity of plants manifested itself through the decrease in yield diminishing due to the improvement of conditions for fertile florets and ear initiations on the vegetative apex, as well as the development of flowers into grains, which contributed to increase in the grain content of the spike. The stimulating effect of selenium on the intensity of photosynthetic processes has been revealed, which showed not only the increase of chlorophylls content, but also the ratio changes of chlorophylls a and b.

Protective effect of selenium on vincristine-induced peripheral neuropathy in PC12 cell line.

Vincristine-induced peripheral neuropathy (VIPN) is the main side effect and major reason for neuropathic pain in cancer survivors treated with vincristine. Vincristine, a chemotherapeutic antimitotic drug, is used frequently in combination chemotherapy. The primary purpose of the current study was to assess the protective effect of sodium selenite (SSe) on VIPN in vitro. Cytotoxicity effects of vincristine were evaluated using PC12 cells as a neuronal model. The cell culture studies were conducted in three groups based on the various treatments, including vincristine, SSe, and co-exposure to both compositions. Cell viability and cell cycle analyses were performed using MTT assay and flow cytometry, respectively. The level of mRNA expression of Bax and Bcl-2 was determined using qRT-PCR. According tothe results, vincristine decreased the survival rate of PC12 cells. After 24 and 48h exposure to different concentrations of vincristine (0.1-20μΜ), the survival rate of PC12 cells decreased as compared to the control group. The results showed that treatment with 5μΜ of vincristine resulted in apoptosis of PC12 cells. Interestingly,co-incubation of these cells with SSe significantly reduced the cell damage induced by vincristine. Furthermore, vincristine induced the inhibition of the G2 phase in PC 12 cells, and using SSe in combination with vincristine eliminated the inhibition of the cell cycle in the G2 phase. Briefly, our in vitro preliminary study showed that SSe might protect PC12 cells from vincristine-induced peripheral neuropathy during chemotherapy.

Selenium ameliorates mercuric chloride-induced brain damage through activating BDNF/TrKB/PI3K/AKT and inhibiting NF-κB signaling pathways

Mercuric chloride (HgCl2), a heavy metal compound, causes neurotoxicity of animals and humans. Selenium (Se) antagonizes heavy metal-induced organ damage with the properties of anti-oxidation and anti-inflammation. Nevertheless, the molecular mechanism underlying the protective effects of sodium selenite (Na2SeO3) against HgCl2-induced neurotoxicity remains obscure. Therefore, the present study aimed to explore the protective mechanism of Na2SeO3 on HgCl2-induced brain damage in chickens. Morphological observations showed that Na2SeO3 alleviated HgCl2-induced brain tissues damage. The results also showed that Na2SeO3 decreased the protein expression of S100 calcium binding protein B (S100B), and increased the levels of nerve growth factors (NGF), doublecortin domain containing 2 (DCDC2), as well as neurotransmitter to reverse HgCl2-induced brain dysfunction. Further, Na2SeO3 attenuated HgCl2-induced oxidative stress by decreasing the level of malondialdehyde (MDA) and increasing the activities of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC). Mechanistically, Na2SeO3 activated the brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase receptor type B (TrKB)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and suppressed the nuclear factor kappa B (NF-κB) signaling pathway to inhibit apoptosis and inflammation caused by HgCl2 exposure. In summary, Na2SeO3 ameliorated HgCl2-induced brain injury via inhibiting apoptosis and inflammation through activating BDNF/TrKB/PI3K/AKT and suppressing NF-κB pathways.

Effect of sodium selenite on synaptic plasticity and neurogenesis impaired by hypothyroidism

Aim of the study We investigated protective effect of sodium selenite (Se) on hypothyroidism-induced impairments in, Morris water maze (MWM), long-term potentiation (LTP) and hippocampal neurogenesis male Wistar rats aged of 2 months. Materials and methods Hypothyroidism was induced by administration of propylthiouracil (Ptu, 1 mg/kg/d) solution to the rats from postnatal day 60 for 81 days with or without Se (0.5mg/kg/d). Neurogenesis was examined by Ki-67 immunohistochemical staining. Se values on plasma and hippocampus were measured with inductively coupled plasma-mass spectrometry (ICP-MS). Results Measurement of fT3 and fT4 levels confirmed that the fT3 levels, but not fT4, in Ptu-treated rats (5435.44±816.05 fg/ml, p < 0.05) has returned to control values (8721.66±2567.68 fg/ml) by Se treatment (8661.65±711.43 fg/ml). Analysis of learning performance in water escape learning task showed that Se supplementation disappeared memory deficit in Ptu-treated rats as shown by significantly decreased time spent in the target quadrant (33.7±0.24% in control group; 26.1±0.48% in Ptu-group, p < 0.05; 33.9±0.44 in Ptu+Se group), although there was no significant difference among groups in any measurement of learning performance on the last day. Considering LTP, Se supplementation improved the deficit in synaptic plasticity in Ptu-treated rats, as shown by significant increase in the excitatory postsynaptic potential slope (% 243±31 in control group; 172±49 in Ptu-group, p < 0.05; 222±65 in Ptu+Se group) without affecting of the impairment in somatic plasticity. Se supplementation did not improve the decrease in the number of progenitor cells in the subgranular layer (SGL) of dentate gyrus (DG) of Ptu treated rats. Conclusions These findings suggest that selenium supplementation in hypothyroid patients may improve learning and memory disorders with different physiological mechanisms. Highlights Se increased serum fT3 levels and hippocampus Se levels in hypothyroid rats. Se attenuated impairment of population spike-LTP in hypothyroid rats Hypothyroidism disrupts neurogenesis process in the dentate gyrus of hippocampus. Se supplementation could not increase new born cells in hypothyroid rats.

Protective Effect of Sodium Selenite on 4-Nonylphenol-Induced Hepatotoxicity and Nephrotoxicity in Rats.

This study was aimed at evaluating the protective effect of sodium selenite (SS) on DNA integrity, antioxidant/oxidant status, and histological changes on 4-nonylphenol (4-NP)-induced toxicity in liver and kidney tissues of rats. Twenty-four adult male Sprague Dawley rats were divided into 4 groups as control, SS, 4-NP, and SS+4-NP group. Control group was untreated. The SS group was supplemented with SS (0.5mg/kg/day) and the 4-NP group was given 4-NP (125mg/kg/day). The rats in the SS+4-NP group received SS followed by 4-NP 1h later at the abovementioned doses. The treatments were administered by oral gavage for 48days. DNA damage was analyzed by comet assay in lymphocytes. Oxidative stress parameters were measured, and histological evaluation was performed in liver and kidney tissues. Results showed that SS administration significantly decreased % Tail DNA and Mean Tail Moment in SS+4-NP group as compared with 4-NP group. Catalase activity in liver was significantly lower in 4-NP group only. SS treatment significantly increased the glutathione level and decreased high malondialdehyde level in tissues of the SS+4-NP group as compared with 4-NP group. Dilation of central vein, ballooning degeneration, vacuolar degeneration, and deterioration in the structure of remark cords in 4-NP-administered were alleviated in rats that received SS supplementation before administration of 4-NP. Moreover, glycogen intensity in hepatocytes and the wall of central vein increased in the SS+4-NP group. In addition, the SS supplementation in the SS+4-NP group decreased glomerular degeneration as well as the width of cavum glomeruli and congestion intensity in the kidney. These results indicate that SS may have a protective effect against 4-NP-induced hepato-nephrotoxicity in rats.

Histological and immunohistochemical study on the effect of Aflatoxin B1 on the ileum of adult male albino rat and possible protective effect of sodium selenite

Background: Aflatoxin B1 is one of dangerous mycotoxins which is produced by Aspergillus fungi. Small intestine especiallyileum is important site for absorption and immunity.Aim: To study histological, ultrastructure and immunohistochemical changes by Aflatoxin B1 on ileum of adult male albinorat and the possible protective effect of sodium selenite.Materials and Methods: Forty adult male albino rats were used, they were divided into four groups, control group (GI),sodium selenite group (GII), Aflatoxin B1 group (GIII), Aflatoxin B1 and sodium selenite group (GIV). Sections were stainedby H&E, Mallory, Alcain blue and proliferating cell nuclear antigen (PCNA). Ultrathin sections were prepared for electronmicroscopic study. Morphometric study for different measurement in ileum were done.Results: Aflatoxin group show marked destruction, disorganization of most villi and crypts, necrosis and vacuolation of coveringand lining cells. Hemorrhage, hyalinization and necrosis in submucosa and muscle layers with heavy lymphocytic infiltrationare seen. Alcain blue stain show significant decrease in intensity. Goblet cells and PCNA + ve cells reveal significant decreasein their numbers. All sections show marked improvement with selenite treatment, ultrastructure changes are in harmony tolight microscope findings.Conclusion: Aflatoxin B1 has destructive histopathological changes on all layers of ileum and sodium selenite has protectiveeffect against this damage.

Silver Nanoparticle Exposure Causes Pulmonary Structural Damage and Mitochondrial Dynamic Imbalance in the Rat: Protective Effects of Sodium Selenite.

BackgroundWith the increased application of Silver nanoparticles (AgNP), its potential concerns to the health of human beings remain to be defined. This study aims to explore the harmful effects of AgNP on lung tissue in animals and to examine the mechanisms of protection achieved by sodium selenite.MethodsSprague-Dawley(SD) rats were exposed to AgNP (200 μL,1mg/mL) through a single intratracheal instillation. Sodium selenite (0.2mg/kg) was i.p. injected. Malondialdehyde (MDA) and glutathione (GSH) were measured using a spectrophotometer. Histological outcomes and ultrastructural changes were assessed by hematoxylin and eosin (HE) staining and electronic microscopy. Caspases and mitochondrial fission and fusion markers were measured by Western blotting.ResultsThe histopathologic findings showed that AgNP significantly increased the thickness of alveolar septa, accumulation of macrophage, and the formation of pulmonary bullae and pulmonary consolidation. Ultrastructural studies showed localization of AgNP inside the mitochondria, hyperplasia and vacuolation of type I and type II alveolar cells, lysis of osmiophilic lamellar bodies, and swollen of the mitochondria. AgNP elevated MDA and reduced GSH levels. AgNP activated caspases-3, increased mitochondrial fission markers Dynamin-related protein 1 (Drp1) and phospho-Drp1(p-Drp1), and decreased fusion proteins optic atrophy 1 (Opa1) and mitofusins 2 (Mfn2). Treatment with sodium selenite for 7 days corrected the AgNP-caused alterations in morphological, ultrastructural, oxidative stress, caspase-3 activation and mitochondrial dynamic imbalance.ConclusionWe conclude that the exposure of AgNP causes lung tissue damage by enhances oxidative stress, activates caspases-3, and triggers mitochondrial dynamic imbalance towards fission. Sodium selenite effectively detoxifies the AgNP-induced damage to the lung tissue by preventing the above alterations.

The protective effect of selenium from heat stress-induced porcine small intestinal epithelial cell line (IPEC-J2) injury is associated with regulation expression of selenoproteins

The present study compared the protective effect of sodium selenite (SS) and selenomethionine (SeMet) on heat stress (HS)-invoked porcine IPEC-J2 cellular damage and integrate potential roles of corresponding selenoprotein. Cells were cultured at 37°C until 80 % confluence and then subjected to four different conditions for 24h: at 37°C (control), 41·5°C (HS), 41·5°C supplied with 0·42 µmol Se/L SS (SS), or SeMet (SeMet). HS significantly decreased cell viability, up-regulated mRNA and protein levels of heat shock protein 70 (HSP70) and down-regulated mRNA and protein levels of tight junction-related proteins (claudin-1 (CLDN-1) and zonula occludens-1 (ZO-1)). HS-induced cell injury was associated with the up-regulation (P < 0·05) of six inflammation-related genes and fourteen selenoprotein encoding genes and down-regulation (P < 0·05) of two inflammation-related genes and five selenoprotein encoding genes. Compared with the HS group, SS and SeMet supplementation resulted in an increase (P < 0·05) in cell viability, decreased (P < 0·05) mRNA expression of HSP70 and six inflammation-related genes and rescue (P < 0·05) of mRNA and protein levels of CLDN-1 and ZO-1. SS and SeMet supplementation changes the expressions of nineteen selenoprotein encoding genes in cells affected by HS. Both Se supplementation significantly recovered the protein level of glutathione peroxidase-1 and increased selenoprotein P in the IPEC-J2 cells under HS, respectively. In summary, Se supplementation alleviated the negative impact of HS on IPEC-J2 cells, and their cellular protective effect was associated with regulation expression of selenoproteins, and SeMet exhibited a better protective effect.

Toxicity of DON on GPx1-Overexpressed or Knockdown Porcine Splenic Lymphocytes In Vitro and Protective Effects of Sodium Selenite.

Deoxynivalenol (DON) is a common contaminant of grain worldwide and is often detected in the human diet and animal feed. Selenium is an essential trace element in animals. It has many biological functions. The role of selenium in the body is mainly orchestrated by selenoprotein. Glutathione peroxidase (GPx) also exists widely in the body and has attracted much attention due to its high antioxidant capacity. In order to explore the effect of the GPx1 gene on toxicity of DON, in this study, we overexpressed or knockdown GPx1 in porcine splenic lymphocytes, then added different concentrations of DON (0.1025, 0.205, 0.41, and 0.82 μg/mL) and sodium selenite (2 μmol/L) to the culture system. Using various techniques, we detected antioxidant function, free radical content, cell apoptosis, and methylation-related gene expression to explore the effect of GPx1 expression on DON-induced cell damage. We also explored whether selenium can antagonize the toxicity of DON in these two cell models and revealed the protective effect of sodium selenite on DON-induced cell damage in GPx1-overexpressing or knockdown splenic lymphocytes. Finally, our findings revealed the following: (1) GPx1 can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes. (2) Na2SeO3 (2 μmol/L) can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes, and this effect is more significant in GPx1-overexpressing cells than in GPx1-knockdown cells. (3) DON can cause oxidative damage, apoptosis, and methylation injury in GPx1-overexpressing or knockdown pig splenic lymphocytes in a concentration-dependent manner. (4) Na2SeO3 (2 μmol/L) can antagonize the toxic effect of DON on GPx1-overexpressing or knockdown pig splenic lymphocytes. Our findings may have important implications for food/feed safety, human health, and environmental protection.

The Molecular Mechanisms of Protective Role of Se on the G0/G1 Phase Arrest Caused by AFB1 in Broiler's Thymocytes.

This research was designed to explore the protective effects of sodium selenite on G0/G1 phase arrest induced by AFB1 in thymocytes of broilers. Two hundred eighty-eight Cobb broilers were divided into control group, + Se group (0.4mg/kg Se), AFB1 group (0.6mg/kg AFB1), and AFB1 + Se group (0.6mg/kg AFB1 + 0.4mg/kg Se). The results revealed that 0.4mg/kg Se supplement in diets could improve the AFB1-induced histological lesions in the thymus consisting of the more vacuoles and nuclear debris in thymic cortical area. The results of flow cytometric detect showed that 0.4mg/kg Se relieved the G0/G1 phase arrest caused by AFB1 in thymocytes. The results of transcription levels of ATM, p53, p21, p27, p15, p16, CyclinD1, CyclinE, Cdk6, Cdk2, and PCNA genes by qRT-PC, and protein expression level of PCNA by immunohistochemistry demonstrated that 0.4mg/kg Se could reduce the adverse effects of AFB1 on these parameters. In conclusion, Se could relieve AFB1-induced G0/G1 phase arrest by p15 (or p16)-CyclinD1/Cdk6, ATM-p53-p21-CyclinE/Cdk2, p27-CyclinE/Cdk2 pathways.

Antagonistic effects of different selenium sources on growth inhibition, oxidative damage, and apoptosis induced by fluorine in broilers

Fluorosis can induce oxidative stress through leading to reactive oxygen species (ROS) generation. Selenium (Se) can eliminate ROS by direct and indirect manners. In this study, therefore, we investigated the possible protective effects of sodium selenite (SS) and selenomethionine (Se-Met) on fluorine (F)-induced oxidative stress in broilers. A total of 720 1-day-old Lingnan Yellow broilers were allotted to 4 groups (6 replicates of 30 birds each group) and fed with basal diet (control group), 800mg/kg F (high F group), 800mg/kg F+0.15mg Se/kg as SS (SS group), or Se-Met (Se-Met group), respectively. The experiment lasted 50 d. High F group significantly decreased (P < 0.05) the average daily gain (ADG) and feed efficiency (FE) in comparison with control group. The contents of ROS, malondialdehyde, 8-hydroxydeoxyguanosine, protein carbonyl, and cysteinyl aspartate specific proteinases 3 in serum, liver, and kidney were higher (P < 0.05) in high F group than those in control group. Compared with control group, the decreased (P < 0.05) activities of glutathione peroxidase (GSH-Px) and cytoplasmic thioredoxin reductase (TrxR1) as well as contents of selenoprotein P (SelP), total protein (TP), and B-cell lymphoma-2 in serum and tissues were observed in high F group. Moreover, the pathological lesions of liver and kidney in high F group were more than those in control group. However, supplementation with SS and Se-Met could improve ADG and FE, increase SelP and TP concentrations, elevate GSH-Px and TrxR1 activities, minimize the changes of oxidative stress and apoptosis parameters as well as ultrastructure of liver and kidney, whereas the effects of Se-Met were better than those of SS. The results indicated that excess F could result in growth inhibition of broilers through inducing oxidative stress and subsequently caused oxidative damage to biological macromolecules and soft tissues as well as apoptosis, whereas dietary SS and Se-Met supplementation could antagonize high F induced growth retardation by inhibiting oxidative stress and a mechanism of apoptosis regulation and the impact was more with Se-Met.

Effect of selenium on testicular damage induced by varicocele in adult male Wistar rats

ProjectVaricocele is an abnormal tortuosity and distension of the veins of the pampiniform plexus in the spermatic cord. It is the most common surgically correctable cause of male infertility. Several studies have revealed the effects of increased oxidative stress on serum, semen, and testicular tissues in patients with varicocele or in animal models. The aim of this study was to investigate the effects of sodium selenite on testicular damage induced by experimental left varicocele in male Wistar rats. ProcedureIn the present study, the effects of oral administration of sodium selenite (at doses of 0.05, 0.1, 0.2, and 0.4mg/kg bw) were assessed in normal and varicocelized rats. ResultsThe varicocelized control rats showed decrease in sperm quality parameters, decreased activity of testes CAT, GPX and SOD, increased levels of MDA, and damage in testicular architecture. Administration of sodium selenite significantly reduced these changes to nearly normal levels, but did not change these parameters in normal rats. Histopathological studies further confirmed the protective effects of sodium selenite on varicocele-induced testicular damage in rats. Administrations of sodium selenite did not change these parameters in normal rats. ConclusionsTaken together, the results of this study suggest that sodium selenite treatment may have beneficial effect on the testes of varicocelized rats.

Sodium selenite prevents suppression of mucosal humoral response by AFB1 in broiler's cecal tonsil.

Aflatoxin B1 (AFB1), the most common mycotoxin in human food and animal feed, produces hepatotoxic, genotoxic and immunosuppressive effects in multiple species. Selenium (Se) has emerged as an important element in the dietary prevention of various toxic agents. The present study was designed to scrutinize the protective effects of sodium selenite on the histological lesions and suppression of mucosal humoral response in the cecal tonsil generated by AFB1. A total of 156 one-day-old broilers were divided into four groups and fed on basal diet (control group), 0.6 mg/kg AFB1 (AFB1 group), 0.4 mg/kg Se supplement (+Se group), and 0.6 mg/kg AFB1 + 0.4 mg/kg Se supplement (AFB1+Se group) respectively for 21 days. Our results showed that 0.4 mg/kg Se supplement in broiler's diets could improve the AFB1-induced histological lesions in the cecal tonsils including the depletion of lymphocytes in the lymphatic nodules as well as the shedding of microvilli in the absorptive cells. Moreover, Se could restore the decreased number of IgA+ cells and expression levels of pIgR, IgA, IgG, and IgM mRNA induced by AFB1 to be close to those in the control group. These results demonstrated that 0.4 mg/kg supplemented dietary Se in the form of sodium selenite could protect the cecal tonsils from the histological lesions and suppression of the mucosal humoral response provoked by 0.6 mg/kg AFB1. Our study may provide new experimental evidences for better understanding of AFB1-induced damage of mucosal immunity and protective effect of Se against this toxin.

Protective Effects of Sodium Selenite and Vitamin-E on LPS Induced Endotoxemia of Rats

Protective Effects of Sodium Selenite and Vitamin-E on LPS Induced Endotoxemia of Rats

Symbiotic effect of sodium selenite and vitamin E against lithium carbonate induced brain toxicity in male rats

Lithium drugs have mainly used in the treatment of psychiatric diseases, therefore many side effects resulting from this metal after used for cure. Sothat in the current study we have to determine the effect of lithium carbonate (Li2CO3) after administration orally for six and eight weeks on the neurotransmitters (dopamine, serotonin) and his to pathological changes in brain tissues in the male rats. Fifty adult male rats weighting 200-250 gm were divided into four groups (10 rats in each group). group one received distilled water and kept as negative control. Group tow received lithium carbonate at dose 4 mg/kg only, group three received lithium carbonate at dose 8 mg/kg only also kept as negative control, group four received lithium carbonate at dose 4 mg/kg with antioxidant solution contain sodium selenite at dose of 2.4 mg/ml and vitamin E at dose of 60 mg/ml daily and group five received lithium carbonate at dose 8 mg/kg with antioxidant solution containing sodium selenite at dose of 2.4 mg/ml and vitamin E at dose of 60 mg/ml daily. Rats after anaesthetized by the mixture of xylazine and ketamine for collocation of serum for biochemical and brain for his to pathological analysis. The results appeared a significant decrease in dopamine and a significant increase of serotonin in the groups of rats treated with lithium carbonate only and intracellular edema, perivascular edema also neurophagia in brain of Li2CO3 treated rats. Co-treatment of rats with vitamin E and sodium selenite results showed a significant increase in dopamine and significant decrease in serotonin with normal tissue structure of the brain. Finally, the results in the current study demonstrated the protective effect of sodium selenite and vitamin E against toxicity by using lithium carbonate.

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

Absence of selenium protection against methylmercury toxicity in harbour seal leucocytes in vitro

Previous studies described high concentrations of mercury (Hg) and selenium (Se) in the blood of harbour seals, Phoca vitulina from the North Sea. In the present study, we evaluated the in vitro potential protective effects of sodium selenite (Na2SeO3) and selenomethionine (SeMet) on cell proliferation of harbour seal lymphocytes exposed to MeHgCl 0.75μM. In vitro exposure of ConA-stimulated T lymphocytes resulted in severe inhibition of DNA synthesis, likely linked to severe loss of mitochondrial membrane potential at 0.75μM. Neither selenite nor SeMet showed a protective effect against MeHg toxicity expressed at the T lymphocyte proliferation level for harbour seals. Selenite and SeMet did not show negative effects regarding lymphocyte proliferation and mitochondrial membrane potential.To conclude, our results clearly demonstrated that MeHg affected in vitro immune cells exposure with no protective effects of selenium at a molar ratio Hg:Se of 1:10 in harbour seals from the North Sea.

Effects of sodium selenite on c-Jun N-terminal kinase signalling pathway induced by oxidative stress in human chondrocytes and c-Jun N-terminal kinase expression in patients with Kashin-Beck disease, an endemic osteoarthritis.

The c-Jun N-terminal kinases (JNK) are members of the mitogen-activated protein kinase family and are activated by environmental stress. Se plays an important role in the biological pathways by forming selenoprotein. Selenoproteins have been shown to exhibit a variety of biological functions including antioxidant functions and maintaining cellular redox balance, and compromise of such important proteins would lead to oxidative stress and apoptosis. We examined the expression levels of JNK in Kashin-Beck disease (KBD) patients, tested the potential protective effects of sodium selenite on tert-butyl hydroperoxide (tBHP)-induced oxidative injury and apoptosis in human chondrocytes as well as its underlying mechanism in this study. We produced an oxidative damage model induced by tBHP in C28/I2 human chondrocytes to test the essential anti-apoptosis effects of Se in vitro. The results indicated that the expression level of phosphorylated JNK was significantly increased in KBD patients. Cell apoptosis was increased and molecule expressions of the JNK signalling pathway were activated in the tBHP-injured chondrocytes. Na2SeO3 protected against tBHP-induced oxidative stress and apoptosis in cells by increasing cell viability, reducing reactive oxygen species generation, increasing Glutathione peroxidase (GPx) activity and down-regulating the JNK pathway. These results demonstrate that apoptosis induced by tBHP in chondrocytes might be mediated via up-regulation of the JNK pathway; Na2SeO3 has an effect of anti-apoptosis by down-regulating the JNK signalling pathway.

Protective effects of sodium selenite on lead nitrate-induced hepatotoxicity in diabetic and non-diabetic rats.

In the present study, the effect of sodium selenite on lead induced toxicity was studied in Wistar rats. Sodium selenite and lead nitrate were administered orally for 28 days to streptozotocin induced diabetic and non-diabetic rats. Eight groups of rats were used in the study: control, sodium selenite, lead nitrate, lead nitrate+sodium selenite, streptozotocin-induced diabetic-control, diabetic-sodium selenite, diabetic-lead nitrate, diabetic-lead nitrate+sodium selenite groups. Serum biochemical parameters, lipid peroxidation, antioxidant enzymes and histopathological changes in liver tissues were investigated in all groups. There were statistically significant changes in liver function tests, antioxidant enzyme activities and lipid peroxidation levels in lead nitrate and sodium selenite+lead nitrate treated groups, also in diabetic and non-diabetic groups. Furthermore, histopathological alterations were demonstrated in same groups. In the present study we found that sodium selenite treatment did not show completely protective effect on diabetes mellitus caused damages, but diabetic rats are more susceptible to lead toxicity than non-diabetic rats.