• 약학회지
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• 제32권4호
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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.

• 약학회지
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• 제29권4호
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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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• 제21권7호
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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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• 제42권6호
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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.

• 한국환경보건학회지
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• 제23권4호
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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.

• 한국수의병리학회지
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• 제5권1호
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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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• 제45권3호
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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.

• 대한화장품학회지
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• 제30권1호
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• pp.73-77
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• 2004

셀레늄을 함유하는 펩타이드(셀레늄 펩타이드)는 셀레늄을 함유하는 배지에서 효모를 배양함으로써 생산 하였다. 효모 단백질의 GPC 분석을 통해서 다양한 크기의 단백질 내 셀레늄 분포를 조사한 결과 셀레늄이 효모 내 단백질에 균일하게 분포하는 것을 확인하였다. 단백질당 셀레늄 양은 배지에 첨가한 셀레늄 양이 증가함에 따라 증가하였고 펩타이드 내의 셀레늄 함량이 높아질수측 항산화 효과 (glutathione peroxidase 유사 활성)가 증가하였다. 단백질 가수분해효소 XIV를 이용하여 여러 분자량의 펩타이드를 생산하였으며 평균 분자량을 GPC로 분석하였다 셀레늄 펩타이드의 glutathione peroxidase (GPx) 활성은 펩타이드의 분자량이 감소할수록 증가하였다. Sodium selenate은 sodium selenite에 비해 효모의 성장 저해를 적게 받았고 단백질 내 셀레늄 함량이 sodium selenite보다 높았다. 이 결과는 효모 배양에 의한 셀레늄 펩타이드의 생산의 가능성과 이를 이용한 항산화 제로서의 응용가능성을 보여주었다.

• BMB Reports
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• 제42권9호
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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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• 제23권1호
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• pp.1-10
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• 1990

셀레늄이 수은, 카드뮴 및 크롬의 세포독성에 미치는 영향을 파악하고자 이들 중금속을 $0.3{mu}M$에서 $10{mu}M$까지 6개 농도로 각각 희석하여 $1.2{mu}M$의 셀레늄과 함께 혈액 배양에 첨가하고, 48시간 경과후 fluorescence-plus-Giemsa 염색에 의해 2차분열 중기의 염색체에서 자매염색분체교환(SCE)현상을 관찰하여, 셀레늄을 첨가하지 않았을 때의 결과와 비교하였다. 셀레늄을 다른 중금속들의 경우와 동일한 농도로 단독 첨가한 경우 SCE빈도는 $5.9{\pm}2.64$회에서 $12.3{\pm}3.99$회의 범위로 변하였고, 수은은 $6.5{\pm}2.70$회에서 $15.7{\pm}2.75$회, 카드뮴은 $6.7{\pm}2.65$회에서 $11.2{\pm}4.13$회, 크롬은 $7.0{\pm}2.58$회에서 $14.9{\pm}6.43$회의 범위로 농도증가에 비례하여 SCE빈도가 상승하였으며, 이때 세포분열지수는 공히 농도증가에 반비례하여 고농도군에서는 현저히 낮았다. 중금속들과 $1.2{mu}M$의 셀레늄을 동시에 첨가시킨 조건에서는 수은의 경우, 셀레늄과 수은의 몰(mol)농도비가 1:1, 1:2, 1:4의 조건에서, 카드뮴의 경우 1:2 및 1:4의 조건에서 SCE빈도의 현저한 감소를 나타냈으나 크롬의 경우는 셀레늄의 첨가와 무관하였으며, 세포분열지수는 전반적으로 셀레늄의 첨가에 별다른 영향을 받지 않았다.