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Pesquisa : D12.125.154.800.500 [Categoria DeCS]
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[PMID]:29371602
[Au] Autor:Gélinas R; Mailleux F; Dontaine J; Bultot L; Demeulder B; Ginion A; Daskalopoulos EP; Esfahani H; Dubois-Deruy E; Lauzier B; Gauthier C; Olson AK; Bouchard B; Des Rosiers C; Viollet B; Sakamoto K; Balligand JL; Vanoverschelde JL; Beauloye C; Horman S; Bertrand L
[Ad] Endereço:Pole of Cardiovascular Research, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels, 1200, Belgium.
[Ti] Título:AMPK activation counteracts cardiac hypertrophy by reducing O-GlcNAcylation.
[So] Source:Nat Commun;9(1):374, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AMP-activated protein kinase (AMPK) has been shown to inhibit cardiac hypertrophy. Here, we show that submaximal AMPK activation blocks cardiomyocyte hypertrophy without affecting downstream targets previously suggested to be involved, such as p70 ribosomal S6 protein kinase, calcineurin/nuclear factor of activated T cells (NFAT) and extracellular signal-regulated kinases. Instead, cardiomyocyte hypertrophy is accompanied by increased protein O-GlcNAcylation, which is reversed by AMPK activation. Decreasing O-GlcNAcylation by inhibitors of the glutamine:fructose-6-phosphate aminotransferase (GFAT), blocks cardiomyocyte hypertrophy, mimicking AMPK activation. Conversely, O-GlcNAcylation-inducing agents counteract the anti-hypertrophic effect of AMPK. In vivo, AMPK activation prevents myocardial hypertrophy and the concomitant rise of O-GlcNAcylation in wild-type but not in AMPKα2-deficient mice. Treatment of wild-type mice with O-GlcNAcylation-inducing agents reverses AMPK action. Finally, we demonstrate that AMPK inhibits O-GlcNAcylation by mainly controlling GFAT phosphorylation, thereby reducing O-GlcNAcylation of proteins such as troponin T. We conclude that AMPK activation prevents cardiac hypertrophy predominantly by inhibiting O-GlcNAcylation.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/genética
Acetilglucosamina/metabolismo
Cardiomegalia/genética
Miocárdio/metabolismo
Miócitos Cardíacos/metabolismo
Transferases de Grupos Nitrogenados/genética
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/deficiência
Acetilglucosamina/farmacologia
Acilação/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Azasserina/farmacologia
Compostos Azo/farmacologia
Cardiomegalia/metabolismo
Cardiomegalia/patologia
Ativação Enzimática/efeitos dos fármacos
Ativadores de Enzimas/farmacologia
Regulação da Expressão Gênica
Glicosilação/efeitos dos fármacos
Ventrículos do Coração/efeitos dos fármacos
Ventrículos do Coração/metabolismo
Ventrículos do Coração/patologia
Masculino
Camundongos
Camundongos Knockout
Miocárdio/patologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/patologia
Transferases de Grupos Nitrogenados/antagonistas & inibidores
Transferases de Grupos Nitrogenados/metabolismo
Norleucina/análogos & derivados
Norleucina/farmacologia
Fosforilação/efeitos dos fármacos
Cultura Primária de Células
Pironas/farmacologia
Ratos
Ratos Wistar
Transdução de Sinais
Tiofenos/farmacologia
Troponina T/genética
Troponina T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (6-diazo-5-oxonorleucine); 0 (A 769662); 0 (Azo Compounds); 0 (Enzyme Activators); 0 (Pyrones); 0 (Thiophenes); 0 (Troponin T); 832C8OV84S (Norleucine); 87299V3Q9W (Azaserine); EC 2.6.- (Nitrogenous Group Transferases); EC 2.6.1.16 (Gfpt1 protein, mouse); EC 2.7.11.1 (AMPK alpha2 subunit, mouse); EC 2.7.11.31 (AMP-Activated Protein Kinases); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02795-4


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[PMID]:27131835
[Au] Autor:Zhou J; Shen X; Lu Q; Zhang M
[Ad] Endereço:Department of Ophthalmology, Rui Jin Hospital, LuWan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai, China (mainland).
[Ti] Título:Thioredoxin-Interacting Protein (TXNIP) Suppresses Expression of Glutamine Synthetase by Inducing Oxidative Stress in Retinal Muller Glia Under Diabetic Conditions.
[So] Source:Med Sci Monit;22:1460-6, 2016 May 01.
[Is] ISSN:1643-3750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Diabetic retinopathy (DR) is a progressive neurodegenerative disease with early-stage symptoms such as dysfunction of Muller cells, which leads to ganglion cell death. Its pathogenesis is probably associated with oxidative stress and a recently discovered protein, thioredoxin-interacting protein (TXNIP). MATERIAL AND METHODS To explore the role of TXNIP in DR, we cultured Muller cells under diabetic conditions, and then used immunohistochemistry, Western blot, and RT-PCR to detect the expression level of TXNIP under diabetic conditions. We demonstrated the expression level of glutamine synthetase (GS) when TXNIP was inhibited. To explore the potential pathway of TXNIP-induced cell damage in DR, we confirmed the role of IL-1ß under diabetic conditions. RESULTS Diabetes induces TXNIP expressions at mRNA levels, but shows the opposite effect on GS. IL-1ß plays an important role in this pathway. Azaserine effectively increased the expression of GS via attenuating the expression of TXNIP. CONCLUSIONS This study demonstrates the role of TXNIP and its mechanism in DR, provides a possible treatment for DR, and lays a new theoretical foundation for the clinical treatment of DR and other diabetic microvascular changes.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Diabetes Mellitus Experimental/enzimologia
Diabetes Mellitus Experimental/patologia
Células Ependimogliais/patologia
Glutamato-Amônia Ligase/metabolismo
Estresse Oxidativo
Retina/patologia
Tiorredoxinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Azasserina/metabolismo
Células Cultivadas
Diabetes Mellitus Experimental/genética
Imunofluorescência
Regulação da Expressão Gênica
Glucose/toxicidade
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Camundongos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Interleukin-1beta); 0 (RNA, Messenger); 0 (Txnip protein, mouse); 52500-60-4 (Thioredoxins); 87299V3Q9W (Azaserine); EC 6.3.1.2 (Glutamate-Ammonia Ligase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160502
[St] Status:MEDLINE


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[PMID]:26878908
[Au] Autor:Lin SH; Liu T; Ming X; Tang Z; Fu L; Schmitt-Kopplin P; Kanawati B; Guan XY; Cai Z
[Ad] Endereço:State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong SAR.
[Ti] Título:Regulatory role of hexosamine biosynthetic pathway on hepatic cancer stem cell marker CD133 under low glucose conditions.
[So] Source:Sci Rep;6:21184, 2016 Feb 16.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cancer was hypothesized to be driven by cancer stem cells (CSCs), but the metabolic determinants of CSC-like phenotype still remain elusive. Here, we present that hexosamine biosynthetic pathway (HBP) at least in part rescues cancer cell fate with inactivation of glycolysis. Firstly, metabolomic analysis profiled cellular metabolome in CSCs of hepatocellular carcinoma using CD133 cell-surface marker. The metabolic signatures of CD133-positive subpopulation compared to CD133-negative cells highlighted HBP as one of the distinct metabolic pathways, prompting us to uncover the role of HBP in maintenance of CSC-like phenotype. To address this, CSC-like phenotypes and cell survival were investigated in cancer cells under low glucose conditions. As a result, HBP inhibitor azaserine reduced CD133-positive subpopulation and CD133 expression under high glucose condition. Furthermore, treatment of N-Acetylglucosamine in part restores CD133-positive subpopulation when either 2.5 mM glucose in culture media or glycolytic inhibitor 2-deoxy-D-glucose in HCC cell lines was applied, enhancing CD133 expression as well as promoting cancer cell survival. Together, HBP might be a key metabolic determinant in the functions of hepatic CSC marker CD133.
[Mh] Termos MeSH primário: Antígeno AC133/metabolismo
Vias Biossintéticas
Carcinoma Hepatocelular/metabolismo
Glucose/metabolismo
Hexosaminas/biossíntese
Neoplasias Hepáticas/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Azasserina/farmacologia
Biomarcadores
Vias Biossintéticas/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular
Glicólise
Seres Humanos
Metabolômica/métodos
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Biomarkers); 0 (Hexosamines); 87299V3Q9W (Azaserine); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160217
[St] Status:MEDLINE
[do] DOI:10.1038/srep21184


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[PMID]:26377577
[Au] Autor:Jiang B; Zhang X; Di D; Luo G; Shi Y; Zhang J; Berggren-Söderlund M; Nilsson-Ehle P; Xu N
[Ad] Endereço:Department of Cardiothoracic Surgery in the Third Affiliated Hospital, Soochow University, Changzhou, 213003, China.
[Ti] Título:Hyperglycemia-induced downregulation of apolipoprotein M expression is not via the hexosamine pathway.
[So] Source:Lipids Health Dis;14:110, 2015 Sep 16.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We previously demonstrated that hyperglycemia could suppress apolipoprotein M (apoM) synthesis both in vivo and in vitro; however, the mechanism of hyperglycemia-induced downregulation of apoM expression is unknown yet. METHODS: In the present study we further examined if hexosamine pathway, one of the most important pathways of glucose turnover, being involved in modulating apoM expression in the hyperglycemia condition. We examined the effect of glucosamine, a prominent component of hexosamine pathway and intracellular mediator of insulin resistance, on apoM expression in HepG2 cells and in rat's models. In the present study we also determined apolipoprotein A1 (apoA1) as a control gene. RESULTS: Our results demonstrated that glucosamine could even up-regulate both apoM and apoA1 expressions in HepG2 cell cultures. The glucosamine induced upregulation of apoM expression could be blocked by addition of azaserine, an inhibitor of hexosamine pathway. Moreover, intravenous infusion of glucosamine could enhance hepatic apoM expression in rats, although serum apoM levels were not significantly influences. CONCLUSIONS: It is concluded that both exogenous and endogenous glucosamine were essential for the over-expression of apoM, which may suggest that the increased intracellular content of glucosamine does not be responsible for the depressed apoM expression at hyperglycemia condition.
[Mh] Termos MeSH primário: Apolipoproteína A-I/genética
Apolipoproteínas/genética
Hiperglicemia/genética
Lipocalinas/genética
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Antimetabólitos Antineoplásicos/farmacologia
Apolipoproteína A-I/metabolismo
Apolipoproteínas/metabolismo
Apolipoproteínas M
Azasserina/farmacologia
Regulação da Expressão Gênica
Glucosamina/administração & dosagem
Glucosamina/metabolismo
Células Hep G2
Seres Humanos
Hiperglicemia/metabolismo
Hiperglicemia/patologia
Infusões Intravenosas
Lipocalinas/metabolismo
Fígado/patologia
Masculino
Ratos
Ratos Sprague-Dawley
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Antimetabolites, Antineoplastic); 0 (Apolipoprotein A-I); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Apom protein, rat); 0 (Lipocalins); 87299V3Q9W (Azaserine); N08U5BOQ1K (Glucosamine)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150918
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-015-0103-5


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[PMID]:23398176
[Au] Autor:Kalipci E; Ozdemir C; Oztas H
[Ad] Endereço:Nevsehir University, Faculty of Engineering & Architecture, Department of Environmental Engineering , Nevsehir, Turkey. ekalipci@hotmail.com
[Ti] Título:Assessing eco-toxicological effects of industrial 2,4-D acid iso-octylester herbicide on rat pancreas and liver.
[So] Source:Biotech Histochem;88(3-4):202-7, 2013 May.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We studied the eco-toxic and carcinogenic effects of a commonly used 2,4-D acid iso-octylester herbicide on rat liver and pancreas. The rats in Group 1 were fed a standard feed and the rats in Group 2 were fed with standard feed to which was added 200 mg/kg/day 2,4-D acid iso-octylester for 16 weeks. Azaserine, 30 mg/kg/body weight, was injected into rats of Groups 3 and 4 to investigate the effects of 2,4-D acid iso-octylester on the development of neoplasms. After feeding the rats with neoplasms in Group 4 with food including 200 mg/kg/day 2,4-D acid iso-octylester for 16 weeks, an autopsy was carried out on all animals. We found that 2,4-D acid iso-octylester caused the formation of atypical cell foci (ACF) in the pancreata and livers of rats. ACF that were formed experimentally by exposure to azaserine had increased diameter, volume and number of atypical cell foci/mm(2) and mm(3) after exposure to 2,4-D acid iso-octylester. Our observations indicated that this herbicide potentially is a cancer initiator.
[Mh] Termos MeSH primário: Ácido 2,4-Diclorofenoxiacético/análogos & derivados
Herbicidas/toxicidade
Fígado/efeitos dos fármacos
Pâncreas/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido 2,4-Diclorofenoxiacético/administração & dosagem
Ácido 2,4-Diclorofenoxiacético/toxicidade
Animais
Azasserina/administração & dosagem
Azasserina/toxicidade
Carcinógenos/administração & dosagem
Carcinógenos/toxicidade
Cocarcinogênese
Herbicidas/administração & dosagem
Fígado/patologia
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/patologia
Masculino
Pâncreas/patologia
Neoplasias Pancreáticas/induzido quimicamente
Neoplasias Pancreáticas/patologia
Ratos
Ratos Wistar
Vesículas Secretórias/efeitos dos fármacos
Vesículas Secretórias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carcinogens); 0 (Herbicides); 25168-26-7 (2,4-dichlorophenoxyacetic acid isooctyl ester); 2577AQ9262 (2,4-Dichlorophenoxyacetic Acid); 87299V3Q9W (Azaserine)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:130419
[Lr] Data última revisão:
130419
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130213
[St] Status:MEDLINE
[do] DOI:10.3109/10520295.2012.758312


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[PMID]:23331184
[Au] Autor:Yildiz H; Oztas H; Yildiz D; Koc A; Kalipci E
[Ad] Endereço:Mustafa Kemal University, Faculty of Science, Department of Biology, Antakya.
[Ti] Título:Inhibitory effects of acetylsalicylic acid on exocrine pancreatic carcinogenesis.
[So] Source:Biotech Histochem;88(3-4):132-7, 2013 May.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated short (6 months) and long (12 months) term inhibitory effects of low (200 ppm) and high (400 ppm) dosages of acetylsalicylic acid (aspirin) on exocrine pancreatic carcinogenesis. It is known that exocrine pancreatic carcinogenesis can be detected by the presence of atypical acinar cell foci (AACF) in pancreas. We investigated possible inhibitory effects of acetylsalicylic acid in an azaserine-treated rat model. AACF were produced in rats by injection with azaserine according to previous studies. Our findings showed that the number, volume and diameter of pancreatic AACF were reduced after acetylsalicylic acid application. These observations suggest that acetylsalicylic acid may exert a protective effect against neoplastic development of pancreatic acinar cells in azaserine injected rats. Our findings corroborate reports in the literature concerning the effects of aspirin in reducing neoplastic development.
[Mh] Termos MeSH primário: Aspirina/administração & dosagem
Neoplasias Pancreáticas/prevenção & controle
[Mh] Termos MeSH secundário: Células Acinares/efeitos dos fármacos
Células Acinares/patologia
Animais
Anti-Inflamatórios não Esteroides/administração & dosagem
Anticarcinógenos/administração & dosagem
Azasserina/antagonistas & inibidores
Azasserina/toxicidade
Carcinógenos/toxicidade
Neoplasias Colorretais/prevenção & controle
Modelos Animais de Doenças
Seres Humanos
Masculino
Pâncreas Exócrino/efeitos dos fármacos
Pâncreas Exócrino/patologia
Neoplasias Pancreáticas/induzido quimicamente
Neoplasias Pancreáticas/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Anticarcinogenic Agents); 0 (Carcinogens); 87299V3Q9W (Azaserine); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:130419
[Lr] Data última revisão:
130419
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130122
[St] Status:MEDLINE
[do] DOI:10.3109/10520295.2012.758779


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[PMID]:23301939
[Au] Autor:Vibjerg Jensen R; Johnsen J; Buus Kristiansen S; Zachara NE; Bøtker HE
[Ad] Endereço:Department of Cardiology, Aarhus University Hospital, Skejby, Aarhus N, Denmark. Rebekka.vibjerg@ki.au.dk
[Ti] Título:Ischemic preconditioning increases myocardial O-GlcNAc glycosylation.
[So] Source:Scand Cardiovasc J;47(3):168-74, 2013 Jun.
[Is] ISSN:1651-2006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Through the hexosamine biosynthetic pathway (HBP) proteins are modified by O-linked-ß-N-acetylglucosamine (O-GlcNAc), which acts as a stress sensor. Augmentation of O-GlcNAc confers cardioprotection against ischemia- reperfusion injury, but its role in ischemic preconditioning (IPC) is unknown. Azaserine and alloxan are unspecific blockers of the HBP and have been used to block the cardioprotective effects of O-GlcNAc. We hypothesized that IPC reduces infarct size and increases O-GlcNAc levels in hearts subjected to ischemia-reperfusion injury, and that these effects could be blocked by azaserine and alloxan. DESIGN: Isolated rat hearts subjected to 40 min global ischemia and 120 min reperfusion were randomized to control, IPC, IPC + azaserine or alloxan, or control + azaserine or alloxan. The effects on infarct size, hemodynamic recovery, myocardial O-GlcNAc levels, and HBP enzyme activities were determined. RESULTS: IPC reduced infarct size, increased O-GlcNAc levels, O-GlcNAc-transferase levels, and O-GlcNAc-transferase activity. Azaserine and alloxan did not block the effect of IPC on O-GlcNAc levels and O-GlcNAc-transferase activity. CONCLUSIONS: IPC increased O-GlcNAc levels though increased O-GlcNAc-transferase expression and activity. Azaserine and alloxan failed to block these effects presumably due to poor specificity and sensitivity of the blockers, and IPC-mediated cardioprotection may therefore still be dependent on O-GlcNAc.
[Mh] Termos MeSH primário: Acetilglucosamina/metabolismo
Precondicionamento Isquêmico Miocárdico
Infarto do Miocárdio/prevenção & controle
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Aloxano/farmacologia
Animais
Azasserina/farmacologia
Modelos Animais de Doenças
Glicosilação
Hemodinâmica
Masculino
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miocárdio/patologia
N-Acetilglucosaminiltransferases/metabolismo
Ratos
Ratos Wistar
Recuperação de Função Fisiológica
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
6SW5YHA5NG (Alloxan); 87299V3Q9W (Azaserine); EC 2.4.1.- (N-Acetylglucosaminyltransferases); EC 2.4.1.- (O-GlcNAc transferase); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:170301
[Lr] Data última revisão:
170301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130111
[St] Status:MEDLINE
[do] DOI:10.3109/14017431.2012.756984


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[PMID]:23292031
[Au] Autor:Teodoro JS; Gomes AP; Varela AT; Duarte FV; Rolo AP; Palmeira CM
[Ad] Endereço:Faculty of Science and Technology, Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
[Ti] Título:Uncovering the beginning of diabetes: the cellular redox status and oxidative stress as starting players in hyperglycemic damage.
[So] Source:Mol Cell Biochem;376(1-2):103-10, 2013 Apr.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Early hyperglycemic insult can lead to permanent, cumulative damage that might be one of the earliest causes for a pre-diabetic situation. Despite this, the early phases of hyperglycemic exposure have been poorly studied. We have previously demonstrated that mitochondrial injury takes place early on upon hyperglycemic exposure. In this work, we demonstrate that just 1 h of hyperglycemic exposure is sufficient to induce increased mitochondrial membrane potential and generation. This is accompanied (and probably caused) by a decrease in the cells' NAD(+)/NADH ratio. Furthermore, we show that the modulation of the activity of parallel pathways to glycolysis can alter the effects of hyperglycemic exposure. Activation of the pentose phosphate pathway leads to diminished effects of glucose on the above parameters, either by removing glucose from glycolysis or by NADPH generation. We also demonstrate that the hexosamine pathway inhibition also leads to a decreased effect of excess glucose. So, this work demonstrates the need for increased focus of study on the reductive status of the cell as one of the most important hallmarks of initial hyperglycemic damage.
[Mh] Termos MeSH primário: Diabetes Mellitus/metabolismo
Hiperglicemia/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: Azasserina/farmacologia
Glucose/metabolismo
Glucose/farmacologia
Glicólise
Células Hep G2/efeitos dos fármacos
Hexosaminas/metabolismo
Seres Humanos
Hiperglicemia/tratamento farmacológico
Hiperglicemia/fisiopatologia
Potencial da Membrana Mitocondrial
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
NAD/metabolismo
NADP/metabolismo
Oxirredução
Via de Pentose Fosfato/efeitos dos fármacos
Carbonilação Proteica
Espécies Reativas de Oxigênio
Tiamina/análogos & derivados
Tiamina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hexosamines); 0 (Reactive Oxygen Species); 0U46U6E8UK (NAD); 53-59-8 (NADP); 87299V3Q9W (Azaserine); IY9XDZ35W2 (Glucose); X66NSO3N35 (Thiamine); Y92OUS2H9B (benphothiamine)
[Em] Mês de entrada:1310
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130108
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-012-1555-9


  9 / 455 MEDLINE  
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[PMID]:23101568
[Au] Autor:Yener Y; Kalipci E; Öztas H; Aydin AD; Yildiz H
[Ad] Endereço:Necmettin Erbakan University, Faculty of Ahmet Kelesoglu Education, Department of Biology Education, Konya, Turkey. yesimyener@selcuk.edu.tr
[Ti] Título:Possible neoplastic effects of acrylamide on rat exocrine pancreas.
[So] Source:Biotech Histochem;88(1):47-53, 2013 Jan.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated whether the acrylamide formed during cooking carbohydrate-rich foods at high temperatures causes neoplastic changes in rat pancreas. Azaserine, which is an amino acid derivative that has the ability to initiate neoplastic changes in rat pancreas, was injected into 14-day-old male rats once a week for three weeks. Acrylamide was given to both azaserine-injected and non-injected rats at doses of 5 and 10 mg/kg/day in drinking water for 16 weeks after which tissue slides were prepared from the pancreata. Pancreas weights and body weights of rats treated with azaserine and acrylamide together increased significantly compared to the other groups. Moreover, the size, average diameter and volume of atypical acinar cell foci that developed in the pancreata of rats treated with azaserine and acrylamide together increased significantly compared to rats treated with either azaserine or acrylamide alone and control groups. Atypical acinar cell adenoma or adenocarcinoma was not observed in the pancreata of rats in any group.
[Mh] Termos MeSH primário: Acrilamida/farmacologia
Testes de Carcinogenicidade
Pâncreas Exócrino/efeitos dos fármacos
Neoplasias Pancreáticas/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Animais
Azasserina/farmacologia
Peso Corporal/efeitos dos fármacos
Testes de Carcinogenicidade/métodos
Masculino
Tamanho do Órgão/efeitos dos fármacos
Pâncreas Exócrino/metabolismo
Pâncreas Exócrino/patologia
Neoplasias Pancreáticas/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
20R035KLCI (Acrylamide); 87299V3Q9W (Azaserine)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121030
[St] Status:MEDLINE
[do] DOI:10.3109/10520295.2012.733028


  10 / 455 MEDLINE  
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[PMID]:22277779
[Au] Autor:Yoshida S; Yokoyama A
[Ad] Endereço:Central Laboratories for Frontier Technology, KIRIN Holdings Co., Ltd., 1-13-5 Fukuura, Kanazawa-ku, Yokohama-shi, Kanagawa 236­0004, Japan. satoshiy@kirin.co.jp
[Ti] Título:Identification and characterization of genes related to the production of organic acids in yeast.
[So] Source:J Biosci Bioeng;113(5):556-61, 2012 May.
[Is] ISSN:1347-4421
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Organic acids contribute to the flavor of many foods and drinks including alcoholic beverages. To study the cellular processes affecting organic acid production, here we screened collections of Saccharomyces cerevisiae deletion mutants and identified 36 yeast mutants forming a yellow halo on YPD plates containing bromocresol purple, indicating that the pH of the medium had been lowered. The disrupted genes encoded TCA cycle enzymes, transcription factors, signal transducers, and ubiquitin-related proteins. Acetate, pyruvate, and succinate are produced by yeast fermentation in rich medium, and their production was affected by mutations of the genes GTR1, GTR2, LIP5, LSM1, PHO85, PLM2, RTG1, RTG2 and UBP3, and also succinate dehydrogenase-related genes including EMI5, SDH1, SDH2, SDH4, TCM62 and YDR379C-A. Among the genes identified, overexpression of only LIP5 affected the production of acetate in S. cerevisiae. However, overexpression of EMI5, LIP5, RTG2 and UBP3 had a significant effect on the production of acetate, citrate, lactate, and succinate in the bottom-fermenting yeast Saccharomyces pastorianus. Furthermore, phenotypic analysis of the S. cerevisiae disruptants involved in organic acid production showed that azaserine, citrate, ethionine, and sulfite are useful compounds by which mutants with altered organic acid production might be selected. Taken together, these results suggest that the regulation of many organic acids might be simultaneously achieved by activation or inactivation of a single gene.
[Mh] Termos MeSH primário: Ácidos/metabolismo
Proteínas de Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Azasserina/metabolismo
Ácido Cítrico/metabolismo
Etionina/metabolismo
Fermentação
Mutação
Saccharomyces/genética
Saccharomyces/metabolismo
Saccharomyces cerevisiae/enzimologia
Succinato Desidrogenase/genética
Succinato Desidrogenase/metabolismo
Sulfitos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acids); 0 (Saccharomyces cerevisiae Proteins); 0 (Sulfites); 2968PHW8QP (Citric Acid); 87299V3Q9W (Azaserine); EC 1.3.99.1 (Succinate Dehydrogenase); WX1BN24WZT (Ethionine)
[Em] Mês de entrada:1304
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120127
[St] Status:MEDLINE
[do] DOI:10.1016/j.jbiosc.2011.12.017



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