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[PMID]:27921518
[Au] Autor:Soleymanifard S; Rostami A; Aledavood SA; Matin MM; Sazgarnia A
[Ad] Endereço:a Medical Physics Research Center, Mashhad University of Medical Sciences , Mashhad , Iran.
[Ti] Título:Increased radiotoxicity in two cancerous cell lines irradiated by low and high energy photons in the presence of thio-glucose bound gold nanoparticles.
[So] Source:Int J Radiat Biol;93(4):407-415, 2017 Apr.
[Is] ISSN:1362-3095
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Gold nanoparticles modified by thio-glucose are believed to increase the toxicity of radiotherapy in human malignant cells. We report the effect of thio-glucose bound gold nanoparticles (Glu-G nanoparticles), 16 nm in size, on two human lung (QU-DB) and breast (MCF7) cancer cell lines combined with kilo and megavoltage X-rays. MATERIALS AND METHODS: The shape and surface characteristics, the size distribution and light absorption spectrum of the prepared nanoparticles were measured by transmission electron microscopy, dynamic light scattering, and ultraviolet-visible spectrophotometry, respectively. The cell uptake was assayed using the atomic absorption spectrometry. Mitochondrial activity, colony formation, and comet assays were applied to assess and compare the enhanced radiotoxicity of 100 KV and 6 MV X-rays, when combined with Glu-G nanoparticles. RESULTS: Glu-G nanoparticles had no significant toxicity for MCF7 and QU-DB cells up to 100 micromolar concentration. Compared to radiation alone, the intracellular uptake of Glu-G nanoparticles resulted in increased inhibition of cell proliferation by 64.1% and 38.7% for MCF7 cells, and 64.4% and 32.4% for QU-DB cells by 100 kVp and 6 MV X-rays, respectively. Comet assay confirmed an increase of DNA damage as a result of combination of 6 MV photons with Glu-G nanoparticles. CONCLUSION: Glu-G nanoparticles have remarkable potential for enhancing radiotoxicity of both low and high energy photons in MCF7 and QU-DB cells.
[Mh] Termos MeSH primário: Aurotioglucose/administração & dosagem
Sobrevivência Celular/efeitos da radiação
Nanopartículas Metálicas/administração & dosagem
Neoplasias Experimentais/radioterapia
Radiossensibilizantes/administração & dosagem
Radioterapia de Alta Energia/métodos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Relação Dose-Resposta à Radiação
Seres Humanos
Células MCF-7
Neoplasias Experimentais/patologia
Fótons/uso terapêutico
Tolerância a Radiação/efeitos dos fármacos
Dosagem Radioterapêutica
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Radiation-Sensitizing Agents); 2P2V9Q0E78 (Aurothioglucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:161207
[St] Status:MEDLINE
[do] DOI:10.1080/09553002.2017.1268282


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[PMID]:27089175
[Au] Autor:Li Q; Wall SB; Ren C; Velten M; Hill CL; Locy ML; Rogers LK; Tipple TE
[Ad] Endereço:1 Neonatal Redox Biology Laboratory.
[Ti] Título:Thioredoxin Reductase Inhibition Attenuates Neonatal Hyperoxic Lung Injury and Enhances Nuclear Factor E2-Related Factor 2 Activation.
[So] Source:Am J Respir Cell Mol Biol;55(3):419-28, 2016 Sep.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxygen toxicity and antioxidant deficiencies contribute to the development of bronchopulmonary dysplasia. Aurothioglucose (ATG) and auranofin potently inhibit thioredoxin reductase-1 (TrxR1), and TrxR1 disruption activates nuclear factor E2-related factor 2 (Nrf2), a regulator of endogenous antioxidant responses. We have shown previously that ATG safely and effectively prevents lung injury in adult murine models, likely via Nrf2-dependent mechanisms. The current studies tested the hypothesis that ATG would attenuate hyperoxia-induced lung developmental deficits in newborn mice. Newborn C3H/HeN mice were treated with a single dose of ATG or saline within 12 hours of birth and were exposed to either room air or hyperoxia (85% O2). In hyperoxia, ATG potently inhibited TrxR1 activity in newborn murine lungs, attenuated decreases in body weight, increased the transcription of Nrf2-regulated genes nicotinamide adenine dinucleotide phosphate reduced quinone oxidoreductase-1 (NQO1) and heme oxygenase 1, and attenuated alterations in alveolar development. To determine the impact of TrxR1 inhibition on Nrf2 activation in vitro, murine alveolar epithelial-12 cells were treated with auranofin, which inhibited TrxR1 activity, enhanced Nrf2 nuclear levels, and increased NQO1 and heme oxygenase 1 transcription. Our novel data indicate that a single injection of the TrxR1 inhibitor ATG attenuates hyperoxia-induced alterations in alveolar development in newborn mice. Furthermore, our data support a model in which the effects of ATG treatment likely involve Nrf2 activation, which is consistent with our findings in other lung injury models. We conclude that TrxR1 represents a novel therapeutic target to prevent oxygen-mediated neonatal lung injury.
[Mh] Termos MeSH primário: Hiperóxia/complicações
Hiperóxia/enzimologia
Lesão Pulmonar/complicações
Lesão Pulmonar/enzimologia
Fator 2 Relacionado a NF-E2/metabolismo
Tiorredoxina Dissulfeto Redutase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Auranofina/farmacologia
Aurotioglucose/farmacologia
Peso Corporal/efeitos dos fármacos
Linhagem Celular
Regulação da Expressão Gênica/efeitos dos fármacos
Heme Oxigenase-1/metabolismo
Hiperóxia/patologia
Lesão Pulmonar/patologia
Camundongos
Camundongos Endogâmicos C3H
Morfogênese/efeitos dos fármacos
NAD(P)H Desidrogenase (Quinona)/metabolismo
Alvéolos Pulmonares/efeitos dos fármacos
Alvéolos Pulmonares/crescimento & desenvolvimento
Alvéolos Pulmonares/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Tiorredoxina Dissulfeto Redutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-E2-Related Factor 2); 0 (RNA, Messenger); 2P2V9Q0E78 (Aurothioglucose); 3H04W2810V (Auranofin); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (Nqo1 protein, mouse); EC 1.8.1.9 (Thioredoxin-Disulfide Reductase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2015-0228OC


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[PMID]:26184149
[Au] Autor:Gandin V; Fernandes AP
[Ad] Endereço:Department of Pharmaceutical and Pharmacological Sciences, University of Padova, Via Marzolo 5, 35131 Padova, Italy. valentina.gandin@unipd.it.
[Ti] Título:Metal- and Semimetal-Containing Inhibitors of Thioredoxin Reductase as Anticancer Agents.
[So] Source:Molecules;20(7):12732-56, 2015 Jul 14.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The mammalian thioredoxin reductases (TrxRs) are a family of selenium-containing pyridine nucleotide disulfide oxidoreductases playing a central role in cellular redox homeostasis and signaling pathways. Recently, these selenoproteins have emerged as promising therapeutic targets for anticancer drug development, often being overexpressed in tumor cells and contributing to drug resistance. Herein, we summarize the current knowledge on metal- and semimetal-containing molecules capable of hampering mammalian TrxRs, with an emphasis on compounds reported in the last decade.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Inibidores Enzimáticos/farmacologia
Proteínas de Neoplasias/antagonistas & inibidores
Tiorredoxina Dissulfeto Redutase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Auranofina/síntese química
Auranofina/farmacologia
Aurotioglucose/síntese química
Aurotioglucose/farmacologia
Inibidores Enzimáticos/síntese química
Seres Humanos
Isoenzimas/antagonistas & inibidores
Isoenzimas/química
Modelos Moleculares
Proteínas de Neoplasias/química
Neoplasias/tratamento farmacológico
Neoplasias/enzimologia
Neoplasias/patologia
Compostos Organoplatínicos/síntese química
Compostos Organoplatínicos/farmacologia
Estresse Oxidativo
Fosfinas/síntese química
Fosfinas/farmacologia
Compostos de Rutênio/síntese química
Compostos de Rutênio/farmacologia
Tiorredoxina Dissulfeto Redutase/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); 0 (Isoenzymes); 0 (Neoplasm Proteins); 0 (Organoplatinum Compounds); 0 (Phosphines); 0 (Ruthenium Compounds); 2P2V9Q0E78 (Aurothioglucose); 3H04W2810V (Auranofin); EC 1.8.1.9 (Thioredoxin-Disulfide Reductase)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150718
[Lr] Data última revisão:
150718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150718
[St] Status:MEDLINE
[do] DOI:10.3390/molecules200712732


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[PMID]:25950356
[Au] Autor:Gowring LE; Kobayashi TT; Lewin-Smith MR
[Ad] Endereço:Department of Dermatology, San Antonio Military Medical Center, San Antonio, TX, USA.
[Ti] Título:Localized chrysiasis, aluminum salt deposition and dystrophic calcification a decade after gold injections.
[So] Source:J Cutan Pathol;42(8):568-73, 2015 Aug.
[Is] ISSN:1600-0560
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Localized chrysiasis is rare and can occur in two settings: after localized or traumatic implantation of elemental gold or gold salts or after localized laser or light therapy in someone who has been previously exposed to systemic gold therapy. We report a unique case of localized chrysiasis with associated aluminum salt deposition and sclerosing lipogranulomas because of previous injections of aurothioglucose (Solganal®). The unique histopathologic findings seen in this case have not been previously reported.
[Mh] Termos MeSH primário: Alumínio/metabolismo
Aurotioglucose/efeitos adversos
Calcinose/induzido quimicamente
Granuloma/induzido quimicamente
[Mh] Termos MeSH secundário: Idoso
Antirreumáticos/administração & dosagem
Antirreumáticos/efeitos adversos
Artrite Reumatoide/tratamento farmacológico
Aurotioglucose/administração & dosagem
Calcinose/metabolismo
Calcinose/patologia
Feminino
Granuloma/metabolismo
Granuloma/patologia
Seres Humanos
Síndrome de Sjogren/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antirheumatic Agents); 2P2V9Q0E78 (Aurothioglucose); CPD4NFA903 (Aluminum)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150814
[Lr] Data última revisão:
150814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150508
[St] Status:MEDLINE
[do] DOI:10.1111/cup.12506


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[PMID]:24114595
[Au] Autor:Wang C; Jiang Y; Li X; Hu L
[Ad] Endereço:Center of Oncology, Second Hospital of Shandong University, Jinan, Shandong, People's Republic of China.
[Ti] Título:Thioglucose-bound gold nanoparticles increase the radiosensitivity of a triple-negative breast cancer cell line (MDA-MB-231).
[So] Source:Breast Cancer;22(4):413-20, 2015 Jul.
[Is] ISSN:1880-4233
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gold nanoparticles (GNPs) have been conceived to cause increased cytotoxicity of radiotherapy in human malignant cells. Greater uptake of GNPs by cells may induce increased radiation effects. Here we report the radiosensitization effect of glucose-capped GNPs (Glu-GNPs) with different sizes (16 nm and 49 nm) on MDA-MB-231 cells in the presence of megavoltage X-rays. METHODS: Transmission electron microscopy (TEM) was used to observe the distribution of Glu-GNPs in cells. Inductively coupled plasma atomic emission spectroscopy (ICP-AES) was used to measure the quantities of Glu-GNPs absorbed by cells. After treatment of Glu-GNPs with a series of concentrations, we used the MTT and clonogenic assays to confirm the radiation enhancement effect of Glu-GNPs on MDA-MB-231 cells. The cell cycle distribution was analyzed by flow cytometry to further explore the mechanisms of enhanced radiosensitivity of Glu-GNPs. RESULTS: TEM showed that Glu-GNPs are mainly distributed in the cytoplasm of cells, including endosomes and lysosomes. ICP-AES indicates that MDA-MB-231 cells absorb more 49-nm Glu-GNPs than 16-nm Glu-GNPs in number (P < 0.05). Glu-GNPs have little cytotoxicity toward MDA-MB-231 cells with a concentration below 20 nM. In the clonogenic assay, the combination of Glu-GNPs with radiation induced a significant growth inhibition, compared with radiation alone (P < 0.05). Moreover 49-nm Glu-GNPs induced much greater radiation effects than 16-nm Glu-GNPs (P < 0.05). Flow cytometry shows that Glu-GNPs can help radiation arrest more cells in the G2/M phase, with greater effect with 49-nm Glu-GNPs than 16-nm Glu-GNPs. CONCLUSIONS: Glu-GNPs can increase the cytotoxicity of radiation toward MDA-MB-231 cells, probably by regulating the distribution of the cell cycle, with more cells in the G2/M phase. The effect of radiation enhancement may be related to the quantities of Glu-GNPs in the cells.
[Mh] Termos MeSH primário: Aurotioglucose/farmacologia
Nanopartículas/química
Radiossensibilizantes/farmacologia
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Neoplasias de Mama Triplo Negativas/radioterapia
[Mh] Termos MeSH secundário: Aurotioglucose/química
Aurotioglucose/farmacocinética
Ciclo Celular/efeitos dos fármacos
Ciclo Celular/efeitos da radiação
Linhagem Celular Tumoral/efeitos dos fármacos
Linhagem Celular Tumoral/efeitos da radiação
Feminino
Citometria de Fluxo
Seres Humanos
Microscopia Eletrônica de Transmissão
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Radiation-Sensitizing Agents); 2P2V9Q0E78 (Aurothioglucose)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150626
[Lr] Data última revisão:
150626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131012
[St] Status:MEDLINE
[do] DOI:10.1007/s12282-013-0496-9


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[PMID]:24295151
[Au] Autor:Britt RD; Velten M; Locy ML; Rogers LK; Tipple TE
[Ad] Endereço:1 Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital , Columbus, Ohio.
[Ti] Título:The thioredoxin reductase-1 inhibitor aurothioglucose attenuates lung injury and improves survival in a murine model of acute respiratory distress syndrome.
[So] Source:Antioxid Redox Signal;20(17):2681-91, 2014 Jun 10.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Inflammation and oxygen toxicity increase free radical production and contribute to the development of acute respiratory distress syndrome (ARDS), which is a significant cause of morbidity and mortality in intensive care patients. We have previously reported increased glutathione (GSH) levels in lung epithelial cells in vitro and attenuated adult murine hyperoxic lung injury in vivo after pharmacological thioredoxin reductase-1 (TrxR1) inhibition. Using a murine ARDS model, we tested the hypothesis that aurothioglucose (ATG) treatment increases pulmonary GSH levels, attenuates lung injury, and decreases mortality in a GSH-dependent manner. RESULTS: Adult mice received a single intratracheal dose of 0.375 µg/g lipopolysaccharide (LPS) 12 h before a single intraperitoneal injection of 25 mg/kg ATG. Control mice received intratracheal and/or intraperitoneal saline. Mice were then exposed to room air or hyperoxia (>95% O2). Lung injury was assessed by bronchoalveolar lavage protein concentrations. Expression of glutamate-cysteine ligase modifier subunit (GCLM), GSH, cytokines, and chemokines was determined. Exposure to LPS/hyperoxia induced inflammation and lung injury. ATG treatment significantly attenuated lung injury, increased lung GCLM expression and GSH levels, and decreased mortality. GSH depletion completely prevented the protective effects of ATG in LPS/hyperoxia-exposed mice. INNOVATION: ATG treatment significantly attenuates lung injury and enhances survival in a clinically relevant murine model of ARDS. The protective effects of ATG are GSH dependent. CONCLUSION: Augmentation of GSH systems by TrxR1 inhibition could represent a promising therapeutic approach to attenuate oxidant-mediated lung injury and improve patient outcomes.
[Mh] Termos MeSH primário: Aurotioglucose/administração & dosagem
Lesão Pulmonar/tratamento farmacológico
Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico
Tiorredoxina Redutase 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Radicais Livres/toxicidade
Glutationa/metabolismo
Seres Humanos
Hiperóxia/metabolismo
Hiperóxia/patologia
Inflamação/induzido quimicamente
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Pulmão/efeitos dos fármacos
Pulmão/patologia
Lesão Pulmonar/induzido quimicamente
Lesão Pulmonar/metabolismo
Camundongos
Oxigênio/toxicidade
Síndrome do Desconforto Respiratório do Adulto/etiologia
Síndrome do Desconforto Respiratório do Adulto/metabolismo
Síndrome do Desconforto Respiratório do Adulto/patologia
Tiorredoxina Redutase 1/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Free Radicals); 2P2V9Q0E78 (Aurothioglucose); EC 1.8.1.9 (TXNRD1 protein, human); EC 1.8.1.9 (Thioredoxin Reductase 1); GAN16C9B8O (Glutathione); S88TT14065 (Oxygen)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131204
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2013.5332


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[PMID]:23800945
[Au] Autor:Ono M; Ogasawara M; Hirose A; Mogami S; Ootake N; Aritake K; Higuchi T; Okamoto N; Sakamoto S; Yamamoto M; Urade Y; Saibara T; Oben JA
[Ad] Endereço:Department of Gastroenterology and Hepatology, Kochi Medical School, Kohasu, Nankoku, Kochi, 783-8505, Japan, onom@kochi-u.ac.jp.
[Ti] Título:Bofutsushosan, a Japanese herbal (Kampo) medicine, attenuates progression of nonalcoholic steatohepatitis in mice.
[So] Source:J Gastroenterol;49(6):1065-73, 2014 Jun.
[Is] ISSN:1435-5922
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Obesity-induced liver disease (nonalcoholic fatty liver disease, NAFLD) is now the commonest cause of chronic liver disease in affluent nations. There are presently no proven treatments for NAFLD or its more severe stage, nonalcoholic steatohepatitis (NASH). Bofutsushosan (BTS), a Japanese herbal (Kampo) medicine, long used as an anti-obesity medicine in Japan and other Asian countries, has been shown to reduce body weight and improve insulin resistance (IR) and hepatic steatosis. The precise mechanism of action of BTS, however, remains unclear. To evaluate the ability of BTS to prevent the development of NASH, and determine the mediators and pathways involved. METHODS: C57BL/6 mice were injected intra-peritoneally with gold-thioglucose and fed a high-fat diet (HF) or HF diet admixed with either 2 or 5 % BTS for 12 weeks. The effectiveness of BTS in attenuating features of NASH and the mechanisms through which BTS attenuated NASH were then assayed through an assessment of the anthropometric, radiological, biochemical and histological parameters. RESULTS: BTS attenuated the progression of NASH through induction of adiponectin and its receptors along with an induction of PPAR-α and PPAR-γ, decreased expression of SREBP-1c, increased hepatic fatty acid oxidation and increased hepatic export of triglycerides. BTS moreover, reduced IR through phosphorylation of the protein kinase, Akt. CONCLUSIONS: BTS through induction of adiponectin signaling and Akt attenuated development of NASH. Identification of the active entity in BTS should allow development of novel treatments for NASH.
[Mh] Termos MeSH primário: Adiponectina/metabolismo
Tecido Adiposo/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Medicina Kampo/métodos
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Obesidade/metabolismo
[Mh] Termos MeSH secundário: Animais
Aurotioglucose/farmacologia
Western Blotting
Dieta Hiperlipídica
Progressão da Doença
Teste de Tolerância a Glucose
Resistência à Insulina
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Reação em Cadeia da Polimerase em Tempo Real
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adiponectin); 0 (Drugs, Chinese Herbal); 0 (bofu-tsusho-san); 2P2V9Q0E78 (Aurothioglucose)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130627
[St] Status:MEDLINE
[do] DOI:10.1007/s00535-013-0852-8


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[PMID]:23603200
[Au] Autor:Segi-Nishida E; Sukeno M; Imoto Y; Kira T; Sakaida M; Tsuchiya S; Sugimoto Y; Okuno Y
[Ad] Endereço:Department of Systems Biosciences for Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, Yoshida Shimoadachi-cho, Sakyo-ku, Kyoto 606-8501, Japan. eri.segi.nishida@pharm.kyoto-u.ac.jp
[Ti] Título:Electroconvulsive seizures activate anorexigenic signals in the ventromedial nuclei of the hypothalamus.
[So] Source:Neuropharmacology;71:164-73, 2013 Aug.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The ventromedial nucleus of the hypothalamus (VMH) plays an important role in feeding and energy homeostasis. Electroconvulsive seizure (ECS) therapy is highly effective in the treatment of several psychiatric diseases, including depression, but may also have beneficial effects in other neurological diseases. Although it has been reported that the neurons of the VMH are strongly activated by ECS stimulation, the specific effects of ECS in this hypothalamic subnucleus remain unknown. To address this issue, we investigated the changes in gene expression in microdissected-VMH samples in response to ECS in mice, and examined the behavioral effects of ECS on feeding behavior. ECS significantly induced the expression of immediate-early genes such as Fos, Fosb, and Jun, as well as Bdnf, Adcyap1, Hrh1, and Crhr2 in the VMH. Given that signals of these gene products are suggested to have anorexigenic roles in the VMH, we also examined the effect of ECS on food intake and body weight. Repeated ECS had a suppressive effect on food intake and body weight gain under both regular and high-fat diet conditions. Furthermore, gold-thioglucose-induced hypothalamic lesions, including the VMH and the arcuate nucleus, abolished the anorexigenic effects of ECS, indicating the requirement for the activation of the hypothalamus. Our data show an effect of ECS on increased expression of anorexigenic factors in the VMH, and suggest a role in the regulation of energy homeostasis by ECS.
[Mh] Termos MeSH primário: Regulação do Apetite
Eletroconvulsoterapia
Proteínas do Tecido Nervoso/biossíntese
Neurônios/metabolismo
Obesidade/terapia
Regulação para Cima
Núcleo Hipotalâmico Ventromedial/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação do Apetite/efeitos dos fármacos
Comportamento Apetitivo/efeitos dos fármacos
Aurotioglucose/toxicidade
Comportamento Animal/efeitos dos fármacos
Dieta Hiperlipídica/efeitos adversos
Comportamento Alimentar/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
Microdissecção
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/patologia
Síndromes Neurotóxicas/complicações
Obesidade/complicações
Obesidade/metabolismo
Obesidade/patologia
Regulação para Cima/efeitos dos fármacos
Núcleo Hipotalâmico Ventromedial/efeitos dos fármacos
Núcleo Hipotalâmico Ventromedial/patologia
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nerve Tissue Proteins); 2P2V9Q0E78 (Aurothioglucose)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:130524
[Lr] Data última revisão:
130524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130423
[St] Status:MEDLINE


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[PMID]:23253150
[Au] Autor:Noguchi T; Makino S; Shinahara M; Nishiyama M; Hashimoto K; Terada Y
[Ad] Endereço:Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Nankoku, Japan.
[Ti] Título:Effects of gold thioglucose treatment on central corticotrophin-releasing hormone systems in mice.
[So] Source:J Neuroendocrinol;25(4):340-9, 2013 Apr.
[Is] ISSN:1365-2826
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic administration of gold thioglucose (GTG) causes a hypothalamic lesion that extends from the ventral part of the ventromedial hypothalamus (VMH) to the dorsal part of the arcuate nucleus (ARC), resulting in hyperphagia and obesity in mice. In the present study, we used in situ hybridisation histochemistry to explore the effects of GTG on the central corticotrophin-releasing hormone (CRH) system, which regulates feeding and energy homeostasis. Type 2 CRH receptor (CRHR-2) mRNA expression decreased by 40% at 8 weeks in the VMH and by 40-60% at 2 and 8 weeks in the ARC after GTG injection. By contrast, CRHR-2 mRNA expression in the hypothalamic paraventricular nucleus (PVN) and lateral septum was unchanged. Urocortin (Ucn) 3 mRNA expression in the perifornical area and medial amygdala decreased, whereas CRH mRNA expression in the PVN increased at 2 and 8 weeks after GTG injection. Ucn 1 mRNA expression in the Edingher-Westphal nucleus and Ucn 2 mRNA expression in the PVN were unchanged. Because Ucn 3 is an anorexigenic and a possible endogenous ligand for VMH CRHR-2, our results suggest that decreased Ucn 3 expression and decreased VMH CRHR-2 expression contribute, in part, to GTG-induced hyperphagia and obesity. To determine whether VMH CRHR-2 mediates the anorexigenic effects of Ucn 3, Ucn 3 was administered i.c.v. and food intake was measured 8 weeks after GTG treatment. Ucn 3 decreased cumulative food intake on days 4-7 after surgery compared to i.c.v. administration of vehicle in control mice. By contrast, the anorexigenic effects of i.c.v. Ucn 3 were abolished in GTG-treated mice. Taken together, our results indicate that the Ucn 3 pathway, which innervates the VMH, is involved in appetite regulation via CRHR-2. It remains to be determined whether CRHR-2 in the ARC has additional roles in appetite regulation by Ucn 3.
[Mh] Termos MeSH primário: Aurotioglucose/farmacologia
Hormônio Liberador da Corticotropina/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores de Hormônio Liberador da Corticotropina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Corticotropin-Releasing Hormone); 2P2V9Q0E78 (Aurothioglucose); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121221
[St] Status:MEDLINE
[do] DOI:10.1111/jne.12011


  10 / 805 MEDLINE  
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[PMID]:22977247
[Au] Autor:Du Y; Zhang H; Lu J; Holmgren A
[Ad] Endereço:Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institute, 17177 Stockholm, Sweden.
[Ti] Título:Glutathione and glutaredoxin act as a backup of human thioredoxin reductase 1 to reduce thioredoxin 1 preventing cell death by aurothioglucose.
[So] Source:J Biol Chem;287(45):38210-9, 2012 Nov 02.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thioredoxin reductase 1 (TrxR1) in cytosol is the only known reductant of oxidized thioredoxin 1 (Trx1) in vivo so far. We and others found that aurothioglucose (ATG), a well known active-site inhibitor of TrxR1, inhibited TrxR1 activity in HeLa cell cytosol but had no effect on the viability of the cells. Using a redox Western blot analysis, no change was observed in redox state of Trx1, which was mainly fully reduced with five sulfhydryl groups. In contrast, auranofin killed cells and oxidized Trx1, also targeting mitochondrial TrxR2 and Trx2. Combining ATG with ebselen gave a strong synergistic effect, leading to Trx1 oxidation, reactive oxygen species accumulation, and cell death. We hypothesized that there should exist a backup system to reduce Trx1 when only TrxR1 activity was lost. Our results showed that physiological concentrations of glutathione, NADPH, and glutathione reductase reduced Trx1 in vitro and that the reaction was strongly stimulated by glutaredoxin1. Simultaneous depletion of TrxR activity by ATG and glutathione by buthionine sulfoximine led to overoxidation of Trx1 and loss of HeLa cell viability. In conclusion, the glutaredoxin system and glutathione have a backup role to keep Trx1 reduced in cells with loss of TrxR1 activity. Monitoring the redox state of Trx1 shows that cell death occurs when Trx1 is oxidized, followed by general protein oxidation catalyzed by the disulfide form of thioredoxin.
[Mh] Termos MeSH primário: Aurotioglucose/farmacologia
Glutarredoxinas/metabolismo
Glutationa/metabolismo
Tiorredoxina Redutase 1/metabolismo
Tiorredoxinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Auranofina/farmacologia
Azóis/farmacologia
Western Blotting
Butionina Sulfoximina/farmacologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Glutationa/antagonistas & inibidores
Células HCT116
Células HeLa
Seres Humanos
Modelos Biológicos
Mutação
Compostos Organosselênicos/farmacologia
Oxirredução/efeitos dos fármacos
Ratos
Espécies Reativas de Oxigênio/metabolismo
Tiorredoxina Redutase 1/antagonistas & inibidores
Tiorredoxina Redutase 1/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Azoles); 0 (Glutaredoxins); 0 (Organoselenium Compounds); 0 (Reactive Oxygen Species); 2P2V9Q0E78 (Aurothioglucose); 3H04W2810V (Auranofin); 40X2P7DPGH (ebselen); 5072-26-4 (Buthionine Sulfoximine); 52500-60-4 (Thioredoxins); EC 1.8.1.9 (Thioredoxin Reductase 1); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:150223
[Lr] Data última revisão:
150223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120915
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M112.392225



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