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[PMID]:29202485
[Au] Autor:Aguirre-Vázquez A; Sampayo-Reyes A; González-Escalante L; Hernández A; Marcos R; Castorena-Torres F; Lozano-Garza G; Taméz-Guerra R; de León MB
[Ad] Endereço:Universidad Autónoma de Nuevo León, UANL, Fac. De Biología, San Nicolás delos Garza, Nuevo León, Mexico.
[Ti] Título:Selenite restores Pax6 expression in neuronal cells of chronically arsenic-exposed Golden Syrian hamsters.
[So] Source:Acta Biochim Pol;64(4):635-639, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Arsenic is a worldwide environmental pollutant that generates public health concerns. Various types of cancers and other diseases, including neurological disorders, have been associated with human consumption of arsenic in drinking water. At the molecular level, arsenic and its metabolites have the capacity to provoke genome instability, causing altered expression of genes. One such target of arsenic is the Pax6 gene that encodes a transcription factor in neuronal cells. The aim of this study was to evaluate the effect of two antioxidants, α-tocopheryl succinate (α-TOS) and sodium selenite, on Pax6 gene expression levels in the forebrain and cerebellum of Golden Syrian hamsters chronically exposed to arsenic in drinking water. Animals were divided into six groups. Using quantitative real-time reverse transcriptase (RT)-PCR analysis, we confirmed that arsenic downregulates Pax6 expression in nervous tissues by 53 ± 21% and 32 ± 7% in the forebrain and cerebellum, respectively. In the presence of arsenic, treatment with α-TOS did not modify Pax6 expression in nervous tissues; however, sodium selenite completely restored Pax6 expression in the arsenic-exposed hamster forebrain, but not the cerebellum. Although our results suggest the use of selenite to restore the expression of a neuronal gene in arsenic-exposed animals, its use and efficacy in the human population require further studies.
[Mh] Termos MeSH primário: Arsênico/toxicidade
Neurônios/efeitos dos fármacos
Fator de Transcrição PAX6/genética
Selenito de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Cerebelo/efeitos dos fármacos
Cerebelo/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Mesocricetus
Neurônios/metabolismo
Neurônios/patologia
Prosencéfalo/efeitos dos fármacos
Prosencéfalo/metabolismo
Testes de Toxicidade Crônica
alfa-Tocoferol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (PAX6 Transcription Factor); H4N855PNZ1 (alpha-Tocopherol); HIW548RQ3W (Sodium Selenite); N712M78A8G (Arsenic)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2017_1607


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[PMID]:29176034
[Au] Autor:Jobeili L; Rousselle P; Béal D; Blouin E; Roussel AM; Damour O; Rachidi W
[Ad] Endereço:Cell and Tissue Bank of Hospices Civils de Lyon, Hôpital Edouard Herriot, Lyon, France.
[Ti] Título:Selenium preserves keratinocyte stemness and delays senescence by maintaining epidermal adhesion.
[So] Source:Aging (Albany NY);9(11):2302-2315, 2017 Nov 25.
[Is] ISSN:1945-4589
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Skin is constantly exposed to environmental factors such as pollutants, chemicals and ultra violet radiation (UV), which can induce premature skin aging and increase the risk of skin cancer. One strategy to reduce the effect of oxidative stress produced by environmental exposure is the application of antioxidant molecules. Among the endogenous antioxidants, selenoproteins play a key role in antioxidant defense and in maintaining a reduced cellular environment. Selenium, essential for the activity of selenoproteins, is a trace element that is not synthesized by organisms and must be supplied by diet or supplementation. The aim of this study is to evaluate the effect of Selenium supplementation on skin aging, especially on keratinocytes, the main cells of the epidermis. Our results demonstrate for the first time to our knowledge, the major role of Selenium on the replicative life span of keratinocytes and on aging skin. Selenium protects keratinocyte stem cells (KSCs) against senescence via preservation of their stemness phenotype through adhesion to the basement membrane. Additionally, Selenium supplementation maintains the homeostasis of skin during chronological aging in our senescent skin equivalent model. Controlled supplementation with Selenium could be a new strategy to protect skin against aging.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Adesão Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Senescência Celular/efeitos dos fármacos
Epiderme/efeitos dos fármacos
Queratinócitos/efeitos dos fármacos
Envelhecimento da Pele/efeitos dos fármacos
Selenito de Sódio/farmacologia
Células-Tronco/efeitos dos fármacos
[Mh] Termos MeSH secundário: Membrana Basal/efeitos dos fármacos
Membrana Basal/metabolismo
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Epiderme/metabolismo
Seres Humanos
Queratinócitos/metabolismo
Fenótipo
Células-Tronco/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.18632/aging.101322


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[PMID]:28823206
[Au] Autor:Balázs C; Rácz K
[Ad] Endereço:Budai Endokrin Központ Budapest, Lövoház u 1-5., 1024.
[Ti] Título:[Diagnostic and therapeutical significance of macro-TSH in patients with Hashimoto's thyroiditis].
[Ti] Título:A makro-TSH diagnosztikus és terápiás jelentosége Hashimoto-thyreoiditises betegekben..
[So] Source:Orv Hetil;158(34):1346-1350, 2017 Aug.
[Is] ISSN:0030-6002
[Cp] País de publicação:Hungary
[La] Idioma:hun
[Ab] Resumo:INTRODUCTION: Structure, importance and incidence and clinical role of macro-TSH not clarified in thyroid diseases. AIM: This study was undertaken to determine the incidence and biological role of macro-TSH in patients with Hashimoto's thyroiditis. METHOD: Blood samples taken from patients with Hashimoto's thyroiditis were screened for the presence of macro-TSH with the polyethylene glycol method and confirmed with protein G agarose absorption test and gel filtration chromatography. Stimulatory capacity of macro-TSH was measured by CHO cells bio-assay. Patients were treated with L-thyroxine (mean 66.5 µg/day) and half of them with selenium (mean 60 µg/day), respectively. RESULTS: 880 patients (728 female, aged 44.8 yr) with Hashimoto's thyroiditis was involved in the study. Macro-TSH was found in the serum of 41 patients (4.6%), the mean TSH 185.4 ± 35 IU/l was before PEG precipitations and after 5.55 ± 1.8 IU/l. Titre of anti-TPO proved to be 445 ± 51 IU/l and gradulally decreased to 212 ± 51 IU/l after one year therapy. Both the precipitation, protein G absorption and gel chromatography supported the presence of anti-TSH antibody in the macro-TSH complex. Stimulatory capacity of macro-TSH on CHO bio-assay was not proved. The macro-TSH was detected in the selenium not treated group for 18 ± 3.2 months, selenium-treated for 12 ± 1.9 months. CONCLUSION: It is concluded that anti-human TSH autoantibodies are a major components of macro-TSH and may cause diagnostic and therapeutical difficulties. The PEG precipitation is a suitable screening method for detection of macro-TSH. Selenium is able to decrease of anti-TPO antibodies and macro-TSH, respectively. When the TSH level is greater than 40.0 IU/l, without the signs of hypothyroidism, the presence of macro-TSH is to be considered. Orv Hetil. 2017; 158(34): 1346-1350.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Doença de Hashimoto/diagnóstico
Tireotropina/sangue
[Mh] Termos MeSH secundário: Adulto
Cromatografia em Gel
Suplementos Nutricionais
Feminino
Doença de Hashimoto/tratamento farmacológico
Seres Humanos
Masculino
Meia-Idade
Polietilenoglicóis
Selenito de Sódio/uso terapêutico
Testes de Função Tireóidea
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 30IQX730WE (Polyethylene Glycols); 9002-71-5 (Thyrotropin); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1556/650.2017.30831


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[PMID]:28807789
[Au] Autor:Dai X; Song R; Xiong Y
[Ad] Endereço:Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission of the people's Rupublic of China, Xi'an Jiaotong University Health Science Center, No. 76 Yanta West Road, Xi'an, Shaanxi 710061, China.
[Ti] Título:The expression of ERK and JNK in patients with an endemic osteochondropathy, Kashin-Beck disease.
[So] Source:Exp Cell Res;359(2):337-341, 2017 Oct 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kashin-Beck disease (KBD) is a chronic, endemic osteochondropathy. Its etiopathogenesis is still obscure until now. Epidemiological observation has shown that low selenium play a crucial role in the pathogenesis of KBD. Extracellular signal-regulated kinases (ERKs) and C-Jun N-terminal kinase (JNK), members of the mitogen-activated protein kinase (MAPK) superfamily, play an important role in cell proliferation and differentiation. Nuclear factor-ĸB (NF-ĸB), an important signaling mediator for inflammatory and immune responses, is involved in the regulation of osteoclastogenesis. In the present study, we investigated the expression of ERK and JNK signal molecular, as well as nuclear factor-ĸB in the pathogenesis of Kashin-Beck disease, evaluated the effect of selenium on ERK signal pathway. The expression levels of ERK and JNK signal pathway, as well as nuclear factor-ĸB were investigated for 218 patients and 209 controls by immunoblot analysis in whole blood. Evaluated the effect of selenium on ERK signal pathway by Na SeO treatment. The protein levels of pRaf-1, pMek1/2 and pErk1/2 decreased significantly in KBD patients, p-JNK and NF-ĸB increased in KBD patients. Furthermore, Na SeO treatment improved the reduction of proteins in ERK signal pathway. These findings indicated that ERK and JNK signaling pathways, as well as the expression level of NF-κB signaling molecular are important contributor to the pathogenesis of KBD. Selenium stimulates the phosphorylation of the ERK signaling pathway.
[Mh] Termos MeSH primário: Cartilagem Articular/metabolismo
Doença de Kashin-Bek/genética
MAP Quinase Quinase 4/genética
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/genética
NF-kappa B/genética
Selênio/deficiência
[Mh] Termos MeSH secundário: Cartilagem Articular/patologia
Estudos de Casos e Controles
Linhagem Celular
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Feminino
Regulação da Expressão Gênica
Seres Humanos
Doença de Kashin-Bek/metabolismo
Doença de Kashin-Bek/patologia
MAP Quinase Quinase 1/genética
MAP Quinase Quinase 1/metabolismo
MAP Quinase Quinase 2/genética
MAP Quinase Quinase 2/metabolismo
MAP Quinase Quinase 4/metabolismo
Masculino
Meia-Idade
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-raf/genética
Proteínas Proto-Oncogênicas c-raf/metabolismo
Transdução de Sinais
Selenito de Sódio/farmacologia
terc-Butil Hidroperóxido/antagonistas & inibidores
terc-Butil Hidroperóxido/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 955VYL842B (tert-Butylhydroperoxide); EC 2.7.1.- (MAP2K2 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.12.2 (MAP Kinase Kinase 1); EC 2.7.12.2 (MAP Kinase Kinase 2); EC 2.7.12.2 (MAP Kinase Kinase 4); EC 2.7.12.2 (MAP2K1 protein, human); H6241UJ22B (Selenium); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28757135
[Au] Autor:Zheng X; Xu W; Sun R; Yin H; Dong C; Zeng H
[Ad] Endereço:State Key Laboratory of Natural and Biomimetic Drugs, Beijing, PR China; Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing 100191, PR China.
[Ti] Título:Synergism between thioredoxin reductase inhibitor ethaselen and sodium selenite in inhibiting proliferation and inducing death of human non-small cell lung cancer cells.
[So] Source:Chem Biol Interact;275:74-85, 2017 Sep 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:New effective treatment for human non-small cell lung cancer (NSCLC) is needed. The thioredoxin (Trx) system composes of thioredoxin reductase (TrxR), Trx and NADPH. In this study, we combined an organic selenium compound--TrxR inhibitor ethaselen (BBSKE) with low dosage sodium selenite to inhibit proliferation and induce death of NSCLC cells, and identified underlying mechanisms. Synergistic anti-proliferation effect of BBSKE and selenite was found in human NSCLC cell lines, A549, NCI-H1299 and NCI-1266. A significant increase of apoptosis, necrosis and autophagy were observed in the group of BBSKE plus selenite in A549 cells. The autophagy induced by BBSKE and selenite inhibited apoptosis and necrosis. In addition, BBSKE plus selenite induced G2/M arrest, which was verified by the alteration of gene and protein expression of cell cycle regulatory complexes. The intracellular enzyme activity of TrxR was remarkably decreased by cotreatment of BBSKE and selenite. Besides, the mRNA and protein level of TrxR1 and Trx1 were significantly inhibited by cotreatment of BBSKE and selenite. HEK 293 cells overexpressing TrxR1 were more sensitive to BBSKE plus selenite. The nuclear translocation of Trx1 and Ref-1, as well as expression of Ref-1 and AP-1 were inhibited by combination treatment. In short, BBSKE synergizes selenite in inhibiting proliferation and inducing death of NSCLC cells; BBSKE combined with selenite may be a treatment strategy for NSCLC.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Compostos Organosselênicos/farmacologia
Selenito de Sódio/farmacologia
Tiorredoxina Dissulfeto Redutase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Células A549
Antineoplásicos/química
Antineoplásicos/farmacologia
Autofagia/efeitos dos fármacos
Compostos Bicíclicos Heterocíclicos com Pontes/química
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/patologia
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Sinergismo Farmacológico
Células HEK293
Seres Humanos
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
Proteínas Associadas aos Microtúbulos/metabolismo
Compostos Organosselênicos/química
Proteínas de Ligação a RNA/metabolismo
Selenito de Sódio/química
Tiorredoxina Dissulfeto Redutase/metabolismo
Tiorredoxinas/genética
Tiorredoxinas/metabolismo
Fator de Transcrição AP-1/genética
Fator de Transcrição AP-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((1,2-bis(1,2-benzisoselenazolone-3(2H)-ketone))ethane); 0 (Antineoplastic Agents); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (MAP1LC3B protein, human); 0 (Microtubule-Associated Proteins); 0 (Organoselenium Compounds); 0 (P62 protein, human); 0 (RNA-Binding Proteins); 0 (Transcription Factor AP-1); 52500-60-4 (Thioredoxins); EC 1.8.1.9 (Thioredoxin-Disulfide Reductase); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE


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[PMID]:28579252
[Au] Autor:Ojeda ML; Carreras O; Sobrino P; Murillo ML; Nogales F
[Ad] Endereço:Department of Physiology, Faculty of Pharmacy, Seville University, 41012 Seville, Spain.
[Ti] Título:Biological implications of selenium in adolescent rats exposed to binge drinking: Oxidative, immunologic and apoptotic balance.
[So] Source:Toxicol Appl Pharmacol;329:165-172, 2017 Aug 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcohol intermittent binge drinking (BD) during adolescence decreases the levels of selenium (Se), a trace element that plays a key biological role against oxidative damage in hepatocytes through different selenoproteins such as the antioxidant enzymes glutathione peroxidases (GPx1 and Gpx4) and selenoprotein P (SelP). In this context, it has been found that GPx4 has an essential antioxidant role in mitochondria modulating the apoptosis and NF-kB activation (a factor intimately related to apoptosis and immune function). To further investigate the effectiveness of selenium supplementation in oxidative balance, inflammation and apoptosis, the present study examined the protective effects of 0.4ppm of dietary selenite administrated to adolescent rats exposed to BD. BD consumption depleted Se deposits in all the tissues studied. In liver, GPx1 activity and expression were decreased leading to protein and lipid hepatic oxidation. Moreover GPx4 and NF-kB expression were also decreased in liver, coinciding with an increase in caspase-3 expression. This hepatic profile caused general liver damage as shown the increased serum transaminases ratio AST/ALT. Proinflammatory serum citokines and chemocines were decreased. Se supplementation therapy used restored all these values, even AST levels. These findings suggest for first time that Se supplementation is a good strategy against BD liver damage during adolescence, since it increases GPx1 and GPx4 expression and avoids NF-kB downregulation and caspase-3 upregulation, leading to a better oxidative, inflammatory and apoptotic liver profile. The therapy proposed could be considered to have a great biological efficacy and to be suitable for BD exposed teenagers in order to avoid future hepatic complications.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Bebedeira/tratamento farmacológico
Suplementos Nutricionais
Hepatopatias Alcoólicas/prevenção & controle
Fígado/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Selenito de Sódio/farmacologia
[Mh] Termos MeSH secundário: Fatores Etários
Alanina Transaminase/sangue
Animais
Anti-Inflamatórios/farmacologia
Aspartato Aminotransferases/sangue
Bebedeira/sangue
Bebedeira/imunologia
Bebedeira/patologia
Caspase 3/metabolismo
Citocinas/sangue
Citoproteção
Modelos Animais de Doenças
Glutationa Peroxidase/metabolismo
Seres Humanos
Mediadores da Inflamação/sangue
Fígado/imunologia
Fígado/metabolismo
Fígado/patologia
Hepatopatias Alcoólicas/sangue
Hepatopatias Alcoólicas/imunologia
Hepatopatias Alcoólicas/patologia
Masculino
Ratos Wistar
Selenoproteínas/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator de Transcrição RelA/metabolismo
Consumo de Álcool por Menores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Rela protein, rat); 0 (Selenoproteins); 0 (Transcription Factor RelA); EC 1.11.1.- (glutathione peroxidase GPX1); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.11.1.9 (glutathione peroxidase 4, rat); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Caspase 3); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


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[PMID]:28552757
[Au] Autor:Imai T; Kurihara T; Esaki N; Mihara H
[Ad] Endereço:Institute for Chemical Research, Kyoto University, Uji, Kyoto 611-0011, Japan; Hyogo Prefectural Institute of Technology, Kobe, Hyogo 654-0037, Japan.
[Ti] Título:Selective fluorescence detection method for selenide and selenol using monochlorobimane.
[So] Source:Anal Biochem;532:1-8, 2017 Sep 01.
[Is] ISSN:1096-0309
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The low redox potential of selenide and selenol is physiologically important, as it confers efficient catalytic abilities to selenoproteins. Quantitative determination of selenol and selenide provide important clues for understanding the metabolism and physiological function of selenium. However, selective detection of selenol and selenide is extremely difficult because of their chemical similarity to thiol and sulfide. In this study, we established a highly sensitive, selective, quantitative, and simple method for detection of selenol and selenide, using a reaction with monochlorobimane (MCB), followed by ethyl acetate extraction of the product syn-(methyl,methyl)bimane. We analyzed selenide production from selenite, catalyzed by human glutathione reductase, and also determined selenide and selenol concentrations in Hepa1-6 cells using the MCB method, to demonstrate its practical applications. This study provides a new tool for selenium detection in biology.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/diagnóstico
Fluorescência
Neoplasias Hepáticas/diagnóstico
Pirazóis/química
Compostos de Selênio/análise
Selenito de Sódio/análise
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/metabolismo
Glutationa Redutase/metabolismo
Seres Humanos
Neoplasias Hepáticas/metabolismo
Camundongos
Pirazóis/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyrazoles); 0 (Selenium Compounds); 0 (selenol); 76421-73-3 (monochlorobimane); EC 1.8.1.7 (Glutathione Reductase); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE


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[PMID]:28476005
[Au] Autor:Tarrahi R; Khataee A; Movafeghi A; Rezanejad F; Gohari G
[Ad] Endereço:Department of Plant Biology, Faculty of Natural Sciences, University of Tabriz, 51666-16471 Tabriz, Iran; Research Laboratory of Advanced Water and Wastewater Treatment Processes, Department of Applied Chemistry, Faculty of Chemistry, University of Tabriz, 51666-16471 Tabriz, Iran.
[Ti] Título:Toxicological implications of selenium nanoparticles with different coatings along with Se on Lemna minor.
[So] Source:Chemosphere;181:655-665, 2017 Aug.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nanoparticles have potential high risks for living organisms in the environment due to their specific qualities and their easy access. In the present study, selenium nanoparticles (Se NPs) with two different coatings (l-cysteine and tannic acid) were synthesized. The characteristics of particles were analyzed using XRD, FT-IR and SEM. The impact of the nanoparticles besides Se , on the aquatic higher plant Lemna minor was evaluated and compared. Entrance of l-cysteine and tannic acid capped Se NPs in the roots of Lemna minor was proved by TEM and fluorescence microscopy. Adverse effects of mentioned NPs and differences of these effects from those by sodium selenite as the ionic form were assessed by a range of biophysicochemical tests. Altogether, the results asserted that Lemna minor was notably poisoned by both capped Se NPs and Se . Thus, growth and photosynthetic pigments were decreased while lipid peroxidation along with total phenol and flavonoid contents were raised. Eventually some changes in enzymatic activities were presented. To sum up the consequences, it can be concluded that all changes occurred due to the plant defense system especially in order to remove reactive oxygen species (ROS) and possible phytotoxicity originated by l- cysteine and tannic acid capped Se NPs in addition to Se . The influence of tannic acid capped Se NPs after sodium selenite is stronger by the means of antioxidant enzymes activity in comparison with l-cysteine capped Se NPs.
[Mh] Termos MeSH primário: Alismatales/efeitos dos fármacos
Araceae/efeitos dos fármacos
Nanopartículas/análise
Selênio/toxicidade
[Mh] Termos MeSH secundário: Alismatales/crescimento & desenvolvimento
Alismatales/imunologia
Araceae/crescimento & desenvolvimento
Araceae/imunologia
Cisteína/química
Peroxidação de Lipídeos/efeitos dos fármacos
Nanopartículas/química
Imunidade Vegetal/efeitos dos fármacos
Espécies Reativas de Oxigênio
Selênio/química
Compostos de Selênio
Selenito de Sódio
Taninos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (Selenium Compounds); 0 (Tannins); H6241UJ22B (Selenium); HIW548RQ3W (Sodium Selenite); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE


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[PMID]:28380525
[Au] Autor:Muegge CR; Brennan KM; Schoonmaker JP
[Ti] Título:Supplementation of organic and inorganic selenium to late gestation and early lactation beef cows effect on progeny feedlot performance and carcass characteristics.
[So] Source:J Anim Sci;95(3):1356-1362, 2017 Mar.
[Is] ISSN:1525-3163
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angus × Simmental cows ( = 48, BW = 594 kg, BCS = 5.26, age = 2.7) pregnant with male fetuses were used to determine the effect of selenium source during the last 80 d of gestation and first 108 d of lactation on progeny feedlot performance. At 203 d of gestation, cows were blocked by BW, breed composition, and calf sire and randomly allotted to 1 of 3 treatments: no supplemental Se, 3 mg/d inorganic Se (sodium selenite), and 3 mg/d organic Se (Sel-plex). Maternal diets were formulated to contain 10.4% CP and 0.90 Mcal/kg NE during gestation and 12.1% CP and 1.01 Mcal/kg NE during lactation. Basal diets contained 0.07 and 0.11 mg/kg Se for gestation and lactation diets, respectively. Diets were fed daily as a total mixed ration, and no additional Se, 3 mg/d Se as sodium selenite, or 3 mg/d Se as Sel-Plex were top-dressed daily. Treatment diets were fed through 108 d postpartum (DPP). At 108 DPP cow-calf pairs were commingled until weaning at 210 DPP. At 28 d postweaning, steers ( = 47, BW = 301 kg) were placed in individual pens and fed a diet formulated to provide 13.9% CP and 1.24 Mcal/kg NE. No supplemental Se was fed; however, basal Se concentration was 0.10 mg/kg. The diet was delivered as a total mixed ration once daily. Steers were slaughtered at a target BW of 625 kg. Steers from cows supplemented with organic Se tended to enter the feedlot heavier ( = 0.06) than steers from cows supplemented with inorganic Se. There was no difference in ADG among treatments ( ≥ 0.73), but steers from organic Se cows tended to spend fewer days on feed compared to steers from inorganic Se cows ( = 0.09). Steers from organic Se cows had a greater overall DMI compared to steers from inorganic Se cows ( = 0.04), but there was no difference in overall G:F ( = 0.49). Dressing percentage was greater for steers from cows fed no Se compared with steers from cows fed either inorganic or organic Se ( = 0.03). Maternal Se source had no effect on HCW, back fat, percentage KPH, LM area, yield grade, marbling score, or quality grade distribution ( ≥ 0.17) of progeny. In conclusion, maternal supplementation with organic Se appears to have a long-term benefit on intake of steer progeny and may result in improvements in growth that could decrease days on feed.
[Mh] Termos MeSH primário: Ração Animal/análise
Bovinos/fisiologia
Suplementos Nutricionais
Selênio/farmacologia
Selenito de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Composição Corporal/efeitos dos fármacos
Cruzamento
Bovinos/crescimento & desenvolvimento
Dieta/veterinária
Feminino
Lactação/efeitos dos fármacos
Masculino
Período Pós-Parto/efeitos dos fármacos
Gravidez
Desmame
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
H6241UJ22B (Selenium); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.2527/jas.2016.0960


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[PMID]:28356430
[Au] Autor:Zhao L; Sun LH; Huang JQ; Briens M; Qi DS; Xu SW; Lei XG
[Ad] Endereço:Department of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, Hubei, China.
[Ti] Título:A Novel Organic Selenium Compound Exerts Unique Regulation of Selenium Speciation, Selenogenome, and Selenoproteins in Broiler Chicks.
[So] Source:J Nutr;147(5):789-797, 2017 May.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A new organic selenium compound, 2-hydroxy-4-methylselenobutanoic acid (SeO), displayed a greater bioavailability than sodium selenite (SeNa) or seleno-yeast (SeY) in several species. This study sought to determine the regulation of the speciation of selenium, expression of selenogenome and selenocysteine biosynthesis and degradation-related genes, and production of selenoproteins by the 3 forms of selenium in the tissues of broiler chicks. Day-old male chicks ( = 6 cages/diet, 6 chicks/cage) were fed a selenium-deficient, corn and soy-based diet [base diet (BD), 0.05 mg Se/kg] or the BD + SeNa, SeY, or SeO at 0.2 mg Se/kg for 6 wk. Plasma, livers, and pectoral and thigh muscles were collected at weeks 3 and 6 to assay for total selenium, selenomethionine, selenocysteine, redox status, and selected genes, proteins, and enzymes. Although both SeY and SeO produced greater concentrations ( < 0.05) of total selenium (20-172%) and of selenomethionine (≤15-fold) in the liver, pectoral muscle, and thigh than those of SeNa, SeO further raised ( < 0.05) these concentrations by 13-37% and 43-87%, respectively, compared with SeY. Compared with the BD, only SeO enhanced ( 0.05) the mRNA of ( ) and ( ) in the liver and thigh (62-98%) and thioredoxin reductase (TXRND) activity in the pectoral and thigh muscles (20-37%) at week 3. Furthermore, SeO increased ( 0.05) the expression of ( ) , GPX4, SELENOP, and SELENOU relative to the SeNa group by 26-207%, and the expression of , GPX4, and SELENOP relative to the SeY group by 23-55% in various tissues. Compared with SeNa or SeY, SeO demonstrated a unique ability to enrich selenomethionine and total selenium depositions, to induce the early expression of and mRNA and TXRND activity, and to enhance the protein production of GPX4, SELENOP, and SELENOU in the tissues of chicks.
[Mh] Termos MeSH primário: Butiratos/farmacologia
Fígado/efeitos dos fármacos
Músculos/efeitos dos fármacos
Compostos de Selênio/farmacologia
Selênio/metabolismo
Selenometionina/metabolismo
Selenoproteínas/metabolismo
[Mh] Termos MeSH secundário: Aminoacil-tRNA Sintetases/metabolismo
Fenômenos Fisiológicos da Nutrição Animal
Animais
Butiratos/metabolismo
Galinhas
Glutationa Peroxidase/metabolismo
Fígado/metabolismo
Masculino
Metionina Sulfóxido Redutases/genética
Metionina Sulfóxido Redutases/metabolismo
Músculos/metabolismo
RNA Mensageiro/metabolismo
Selênio/deficiência
Compostos de Selênio/metabolismo
Selenoproteínas/genética
Selenito de Sódio/farmacologia
Tiorredoxina Dissulfeto Redutase/metabolismo
Leveduras
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxy-4-methylselenobutanoic acid); 0 (Butyrates); 0 (RNA, Messenger); 0 (Selenium Compounds); 0 (Selenoproteins); 964MRK2PEL (Selenomethionine); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.8.1.9 (Thioredoxin-Disulfide Reductase); EC 1.8.4.- (Methionine Sulfoxide Reductases); EC 6.1.1.- (Amino Acyl-tRNA Synthetases); H6241UJ22B (Selenium); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.3945/jn.116.247338



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