• YAKHAK HOEJI
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• v.32 no.4
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• pp.287-293
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• 1988

Oxygen free radical have recently been found to mediate cell injury after ischemia in the kidney. The purpose of our study was to determine whether selenium had an effect on damge mediated by oxygen free radical in inorganic mercury induced renal failure, toxic model of renal failure. Toxic renal failure model was produced by subcutaneous injection of mercuric chloride (4mg/kg) once a day for 7 consecutive days. In additionally, coadministration of sodium selenite (1mg/kg) was performed by the same condition. As a consequence of this study, we were able to detect partially unequivocal role of selenium as below dipicted. The combination of sodium selenite showed that markedly inhibited production of superoxide radical in mercuric chloride alone. On the other hand, combined sodium selenite was unable to enhance against significantly lowered superoxide dismutase activity after mercuric chloride insult. However, simultaneous administration of sodium selenite was inclined to induce mitochondrial superoxide dismutase and catalase.

• YAKHAK HOEJI
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• v.29 no.4
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• pp.223-226
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• 1985

0.1%-Merthiolate solutions were applied to rats with or without sodium selenite. Rat organs were excised under ether anesthesia. Mercury contents in rat tissues were determined by quartz tube combustion gold amalgamation method. Mercury contents were accumulated at about 3-fold in the brain, 143-fold in the kidney, 62-fold in the blood cell, 22-fold in the liver than those of untreated rats respectively, on the 1st day after application of mert iolate for 7 days. On the other hand, the addition of sodium selenite caused a shift in the tissue mercury distribution. Our study showed that simultaneous administration of sodium selenite increased the accumulation of mercury in the brain, but became to decrease it after 9 days, while decreased it in the kidney, but grew to increase it, respectively.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.7
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• pp.1048-1052
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• 2008

The objective of this study was to determine the effect of sodium selenite and zinc-L-selenomethionine on performance and egg Se concentration in laying hens. Two hundred and twenty-four CP Browns aged 71 weeks were divided according to a $2{\times}3$ factorial in a completely randomized design. One more group without additional Se supplementation was used as a negative control. Each treatment consisted of four replicates and each replicate contained eight laying hens. The dietary treatments were T1: basal diet; T2, T3 and T4: basal diets plus 0.3, 1.0 and 3.0 mg Se from sodium selenite/kg, respectively; T5, T6 and T7: basal diets plus 0.3, 1.0 and 3.0 mg Se from zinc-L-selenomethionine/kg, respectively. The findings revealed that feed conversion rate/kg eggs, egg production, egg weight, Haugh units and eggshell thickness were not affected by source and level of Se (p>0.05). Increasing level of dietary Se significantly increased (p<0.05 the Se content of eggs. Zinc-L-selenomethionine markedly increased p<0.05 egg Se concentration as compared with sodium selenite. The results indicated that Se source did not influence performance of laying hens. However, zinc-L-selenomethionine increased p<0.05 egg Se concentration more than sodium selenite.

• BMB Reports
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• v.42 no.6
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• pp.361-366
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• 2009

It was reported that high doses of sodium selenite can induce apoptosis of cancer cells, but the molecular mechanisms are poorly understood. Manganese superoxide dismutase (MnSOD) converts superoxide radical to hydrogen peroxide within the mitochondrial matrix and is one of the most important antioxidant enzymes. In this study, we showed that 20 ${\mu}M$ sodium selenite could alter subcellular distribution of MnSOD, namely a decrease in mitochondria and an increase in cytosol. The alteration of subcellular distribution of MnSOD is dependent on the production of superoxide induced by sodium selenite.

• Journal of Environmental Health Sciences
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• v.23 no.4
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• pp.26-32
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• 1997

To evaluate the cytogenetic toxicity, of cadmium and the reducing effect of selenium or zinc on cadmium toxicity, the induction of SCEs in cultured human lymphocytes by the concentraion of 0.5 $\mu$M to 16.0 $\mu$M of cadmium chloride and those of cadmium chloride combined with sodium selenite or zinc chloride 1.2 $\mu$M, respectively was investigated. The induction of SCEs by cadmium chloride in the range of 0.5 $\mu$M to 16.0 $\mu$M increased in a dose-dependent manner. A notable increase in SCEs by sodium selenite as well as zinc chloride was also observed. However, the frequency of SCEs by cadmium chloride was inhibited by the simultaneous addition of sodium selenite and zinc chloride 1.2 $\mu$M, respectively. The mitotic index significantly decreased in higher concentration of cadmium chloride but not was significantly different in any concentration of cadmium chloride with the simultaneous addition of sodium selenite or zinc chloride. The results showed that the decreased additive SCE effect was observed when induced by the combined treatment which could suggest that sodium selenite and zinc chloride have a protective effect on cadmium chloride.

• Korean Journal of Veterinary Pathology
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• v.5 no.1
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• pp.23-28
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• 2001

This study was conducted to assess the chemopreventive effects of sodium selenite in the rat medium-term multi-organ bioassay using a DMBDD model (DEN+MNU+BBN+DMH+DHPN). Seventy five,6-week-old, male SD rats were divided into 3 groups. The animals in group 1 received DEN(diethylnitrosamine,100 mg/kg bw, single i.p., in saline), MNU (N-methyl-nitrosourea,20 mg/kg bw, i.p.,4 times for 2 weeks), BBN (N-butyl-N-(4-hydroxybutyl) nitrosamine, 0.2% in drinking water for 2 weeks), DMH (1,2-dimethylhydrazine, 40 mg/kg bw, s.c., in saline.4 times (or 2 weeds), and DHPN (N-bis(2-hydroxy-pro-pal)nitrosamine,0.1% in drinking water for 2 weeks), then were placed on sodium selenite (4 ppm in drinking water) for 22 weeks from weeks 4 to 26. The animals in group 2 were given DMBDD alone. The animals in group 3 were given sodium selenite alone. Animals were sacrificed at week 12 for ACF quantitative analysis and at week 26 for tumor induction. The body weights in the group 1 were significantly decreased compared with those of group 2. The tumor multiplicities of large intestine in the group 1 were significantly decreased compared with those of group 2 (P<0.05). These results indicate that sodium selenite may have a potential as chemopreventive agents of colon carcinogenesis.

• BMB Reports
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• v.45 no.3
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• pp.194-199
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• 2012

Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at $Ser^{308}$. We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at $Ser^{308}$ serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.30 no.1
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• pp.73-77
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• 2004

Selenium containing peptide was produced by culturing yeast with selenium, Selenium was broadly incorporated in the various size of proteins based on the GPC analysis of the total yeast protein. The ratio of selenium to protein increased with the concentration of added selenium in the culture medium. Antioxidant activity (glutathione peroxidase-like activity) was proportional to the concentration of selenium concentration in the peptide. Different size of proteins were obtained by hydrolyzing the total yeast protein by protease XIV. Average molecular weight of selenium peptide was analyzed by GPC. Glutathione peroxidase (GPx) activity of the selenium peptide increased as the size of peptide decreased. Sodium selenite had strong inhibition on the yeast growth than sodium selenate. The ratio of selenium to protein was higher with sodium selenate than with sodium selenite. These results showed the potentials of selenium peptide production by yeast cultivation.

• BMB Reports
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• v.42 no.9
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• pp.599-604
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• 2009

Selenium possesses the chemotherapeutic feature by inducing apoptosis in cancer cell with trivial side effects on normal cells. However, the mechanism in which is not clearly understood. Emerging evidence indicates the overlaps between the autophagy and the apoptosis. In this study, we have investigated the role of autophagy in selenium-induced apoptosis in NB4 cells. We find that autophagy is suppressed in NB4 cells treated by sodium selenite, as measured by electron microscope, acridine orange staining and western blot. Moreover, selenite combined with autophagy inhibitor contributes to the up-regulation of apoptosis, while the PI3K/Akt signaling pathway is down- regulated. Consistently, when the inhibitor of PI3K was applied, the autophagic level significantly decreased. In summary, sodium selenite increases NB4 cell apoptosis by autophagy inhibition through PI3K/Akt, and the inhibition of autophagy contributes to the up-regulation of apoptosis.

• Journal of Preventive Medicine and Public Health
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• v.23 no.1 s.29
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• pp.1-10
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• 1990

The protective effect of sodium selenite($Na_2SeO_3$) against the cytogenetic toxicity of heavy metals was investigated on human whole-blood cultures in relation to induction of sister chromatid exchange (SCE) in secondary metaphase chromosome. Methylmercury chloride($CH_3HgCl$), cadmium chloride($CdCl_2$), potassium dichromate($K_2Cr_2O_7$), and sodium selenite caused to the typically dose-dependent increase in sister chromatid exchanges (SCEs) by the concentrations ranging from $0.3{\mu}M\;to\;10{mu}M$. However, the inductions of sister chromatid exchanges by methylmercury chloride or cadmium chloride were inhibited by the simultaneous addition of sodium selenite $1.2{mu}M$. The frequencies of SCE were decreased to the level of control in the molar ratios as 2:1, 1:1, 1:2, and 1:4 of selenium selenite vs. methylmercury chloride, and as 1:1 and 1:2 of selenium selenite vs. cadmium chloride, while the frequencies of SCE induced by potassium dichromate were not changed by the addition of sodium selenite in culture condition. Mitotic indices were decreased in the higher concentrations of chemicals and not significantly changed by the simultaneous addition of sodium selenite to the culture condition containing each chemicals.