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Yang Yang - One of the best experts on this subject based on the ideXlab platform.
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The subcellular distribution of MnSOD alters during Sodium Selenite-induced apoptosis.
BMB reports, 2009Co-Authors: Liying Guan, Qian Jiang, Fang Huang, Yun Ren, Yang YangAbstract: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 microM 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.
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Sodium Selenite induces apoptosis in acute promyelocytic leukemia-derived NB4 cells through mitochondria-dependent pathway.
Oncology Research, 2009Co-Authors: Liying Guan, Tao Yang, Yang Yang, Hua DongAbstract:Our previous study has shown that Sodium Selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Δψm disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by Sodium Selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9 , but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay Sodium Selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of Δψm disruption and apoptosis by Sodium Selenite. Our findings here demonstrate that Sodium Selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Δψm disruption, release of cytochrome c, and consequent initiation of caspase cascade.
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Sodium Selenite induces apoptosis in acute promyelocytic leukemia derived nb4 cells through mitochondria dependent pathway
Oncology Research, 2009Co-Authors: Bingshe Han, Liying Guan, Hua Dong, Tao Yang, Yang Yang, Yun Ren, Wei Wei, Fangyuan Hua, Tingming Cao, Huazhen PanAbstract:Our previous study has shown that Sodium Selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Deltapsim disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by Sodium Selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9, but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay Sodium Selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of deltapsim disruption and apoptosis by Sodium Selenite. Our findings here demonstrate that Sodium Selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Deltapsim disruption, release of cytochrome c, and consequent initiation of caspase cascade.
Liying Guan - One of the best experts on this subject based on the ideXlab platform.
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The subcellular distribution of MnSOD alters during Sodium Selenite-induced apoptosis.
BMB reports, 2009Co-Authors: Liying Guan, Qian Jiang, Fang Huang, Yun Ren, Yang YangAbstract: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 microM 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.
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Sodium Selenite induces apoptosis in acute promyelocytic leukemia-derived NB4 cells through mitochondria-dependent pathway.
Oncology Research, 2009Co-Authors: Liying Guan, Tao Yang, Yang Yang, Hua DongAbstract:Our previous study has shown that Sodium Selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Δψm disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by Sodium Selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9 , but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay Sodium Selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of Δψm disruption and apoptosis by Sodium Selenite. Our findings here demonstrate that Sodium Selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Δψm disruption, release of cytochrome c, and consequent initiation of caspase cascade.
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Sodium Selenite induces apoptosis in acute promyelocytic leukemia derived nb4 cells through mitochondria dependent pathway
Oncology Research, 2009Co-Authors: Bingshe Han, Liying Guan, Hua Dong, Tao Yang, Yang Yang, Yun Ren, Wei Wei, Fangyuan Hua, Tingming Cao, Huazhen PanAbstract:Our previous study has shown that Sodium Selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Deltapsim disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by Sodium Selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9, but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay Sodium Selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of deltapsim disruption and apoptosis by Sodium Selenite. Our findings here demonstrate that Sodium Selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Deltapsim disruption, release of cytochrome c, and consequent initiation of caspase cascade.
Hua Dong - One of the best experts on this subject based on the ideXlab platform.
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Sodium Selenite induces apoptosis in acute promyelocytic leukemia-derived NB4 cells through mitochondria-dependent pathway.
Oncology Research, 2009Co-Authors: Liying Guan, Tao Yang, Yang Yang, Hua DongAbstract:Our previous study has shown that Sodium Selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Δψm disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by Sodium Selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9 , but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay Sodium Selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of Δψm disruption and apoptosis by Sodium Selenite. Our findings here demonstrate that Sodium Selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Δψm disruption, release of cytochrome c, and consequent initiation of caspase cascade.
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Sodium Selenite induces apoptosis in acute promyelocytic leukemia derived nb4 cells through mitochondria dependent pathway
Oncology Research, 2009Co-Authors: Bingshe Han, Liying Guan, Hua Dong, Tao Yang, Yang Yang, Yun Ren, Wei Wei, Fangyuan Hua, Tingming Cao, Huazhen PanAbstract:Our previous study has shown that Sodium Selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Deltapsim disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by Sodium Selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9, but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay Sodium Selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of deltapsim disruption and apoptosis by Sodium Selenite. Our findings here demonstrate that Sodium Selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Deltapsim disruption, release of cytochrome c, and consequent initiation of caspase cascade.
Miroslav Chovanec - One of the best experts on this subject based on the ideXlab platform.
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Rad52 has a role in the repair of Sodium Selenite-induced DNA damage in Saccharomyces cerevisiae.
Mutation research, 2008Co-Authors: Lucia Letavayová, Danuša Vlasáková, Viera Vlčková, J. Brozmanová, Miroslav ChovanecAbstract:Selenium (Se) is a chemo-preventive agent that has been shown to have a protective role against cancer. The inorganic form of Se, Sodium Selenite (Na2SeO3), has frequently been included in various chemo-prevention studies, and this commercially available form of Se is used as dietary supplement by the public. Because high doses of this Se compound can be toxic, the underlying molecular mechanisms of Sodium Selenite toxicity need to be elucidated. Recently, we have reported that Sodium Selenite is acting as an oxidizing agent in the budding yeast Saccharomyces cerevisiae, producing oxidative damage to DNA. This pro-oxidative activity of Sodium Selenite likely accounted for the observed DNA double-strand breaks (DSB) and yeast cell death. In this study we determine the genetic factors that are responsible for repair of Sodium Selenite-induced DSB. We report that the Rad52 protein is indispensable for repairing Sodium Selenite-induced DSB, suggesting a fundamental role of homologous recombination (HR) in this repair process. These results provide the first evidence that HR may have a fundamental role in the repair of Sodium Selenite-induced toxic DNA lesions.
Jeffery O. Hall - One of the best experts on this subject based on the ideXlab platform.
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Comparative oral dose toxicokinetics of Sodium Selenite and selenomethionine.
Journal of applied toxicology : JAT, 2016Co-Authors: T. Zane Davis, Asheesh K. Tiwary, Bryan L. Stegelmeier, Kip E. Panter, James A. Pfister, Jeffery O. HallAbstract:Selenium (Se) poisoning by different forms of Se occurs in the United States. However, the toxicokinetics of different selenocompounds after oral ingestion is not well documented. In this study the toxicokinetics of Se absorption, distribution and elimination were determined in serum and whole blood of lambs that were orally dosed with increasing doses of Se as Sodium Selenite (inorganic Se) or selenomethionine (SeMet, organic Se). Thirty-two lambs were randomly assigned to eight treatment groups, with four animals per group. Se was administered at 1, 2 or 3 mg kg-1 body weight, as either Sodium Selenite or SeMet with proper control groups. Blood and serum were collected at predetermined time points for 7 days post-dosing. Resulting Se concentrations in both serum and whole blood from SeMet treatment groups were significantly greater than those given equimolar doses of Se as Sodium Selenite. Se concentrations in serum and whole blood of lambs dosed with SeMet peaked at significantly greater concentrations when compared with lambs dosed with equimolar doses of Sodium Selenite. Based on the serum and whole blood kinetics, the rate of Se absorption was greater for SeMet than for Sodium Selenite although rates of absorption for both Se forms decreased with increasing dose. The rates of Se elimination increased with dose. These results demonstrate that SeMet has a greater absorption rate and a similar retention time resulting in a greater area under the curve and thus bioavailability than Sodium Selenite, which must be considered in both overdose and nutritional exposures. Published 2016. This article is a U.S. Government work and is in the public domain in the USA.
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Comparative toxicosis of Sodium Selenite and selenomethionine in lambs.
Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians Inc, 2006Co-Authors: Asheesh K. Tiwary, Bryan L. Stegelmeier, Kip E. Panter, Lynn F. James, Jeffery O. HallAbstract:Excess consumption of selenium (Se) accumulator plants can result in selenium intoxication. The objective of the study reported here was to compare the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (Sodium Selenite). Lambs were orally administered a single dose of selenium as either Sodium Selenite or selenomethionine and were monitored for 7 days, after which they were euthanized and necropsied. Twelve randomly assigned treatment groups consisted of animals given 0, 1, 2, 3, or 4 mg of Se/kg of body weight as Sodium Selenite, or 0, 1, 2, 3, 4, 6, or 8 mg of Se/kg as selenomethionine. Sodium Selenite at dosages of 2, 3, and 4 mg/kg, as well as selenomethionine at dosages of 4, 6, and 8 mg/kg resulted in tachypnea and/or respiratory distress following minimal exercise. Severity and time to recovery varied, and were dose dependent. Major histopathologic findings in animals of the high-dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Analysis of liver, kidney cortex, heart, blood, and serum revealed linear, dose-dependent increases in selenium concentration. However, tissue selenium concentration in selenomethionine-treated lambs were significantly greater than that in lambs treated with equivalent doses of Sodium Selenite. To estimate the oxidative effects of these selenium compounds in vivo, liver vitamin E concentration also was measured. Sodium Selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Results of this study indicate that the chemical form of the ingested Se must be known to adequately interpret tissue, blood, and serum Se concentrations.
