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[PMID]:29298345
[Au] Autor:Siegel D; Dehn DD; Bokatzian SS; Quinn K; Backos DS; Di Francesco A; Bernier M; Reisdorph N; de Cabo R; Ross D
[Ad] Endereço:Department of Pharmaceutical Sciences, Skaggs School of Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
[Ti] Título:Redox modulation of NQO1.
[So] Source:PLoS One;13(1):e0190717, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NQO1 is a FAD containing NAD(P)H-dependent oxidoreductase that catalyzes the reduction of quinones and related substrates. In cells, NQO1 participates in a number of binding interactions with other proteins and mRNA and these interactions may be influenced by the concentrations of reduced pyridine nucleotides. NAD(P)H can protect NQO1 from proteolytic digestion suggesting that binding of reduced pyridine nucleotides results in a change in NQO1 structure. We have used purified NQO1 to demonstrate the addition of NAD(P)H induces a change in the structure of NQO1; this results in the loss of immunoreactivity to antibodies that bind to the C-terminal domain and to helix 7 of the catalytic core domain. Under normal cellular conditions NQO1 is not immunoprecipitated by these antibodies, however, following treatment with ß-lapachone which caused rapid oxidation of NAD(P)H NQO1 could be readily pulled-down. Similarly, immunostaining for NQO1 was significantly increased in cells following treatment with ß-lapachone demonstrating that under non-denaturing conditions the immunoreactivity of NQO1 is reflective of the NAD(P)+/NAD(P)H ratio. In untreated human cells, regions with high intensity immunostaining for NQO1 co-localize with acetyl α-tubulin and the NAD+-dependent deacetylase Sirt2 on the centrosome(s), the mitotic spindle and midbody during cell division. These data provide evidence that during the centriole duplication cycle NQO1 may provide NAD+ for Sirt2-mediated deacetylation of microtubules. Overall, NQO1 may act as a redox-dependent switch where the protein responds to the NAD(P)+/NAD(P)H redox environment by altering its structure promoting the binding or dissociation of NQO1 with target macromolecules.
[Mh] Termos MeSH primário: NAD(P)H Desidrogenase (Quinona)/metabolismo
[Mh] Termos MeSH secundário: Domínio Catalítico
Linhagem Celular
Eletroforese em Gel de Poliacrilamida
Técnicas de Silenciamento de Genes
Seres Humanos
Imunoprecipitação
Espectrometria de Massas
NAD(P)H Desidrogenase (Quinona)/genética
Naftoquinonas/farmacologia
Eletroforese em Gel de Poliacrilamida Nativa
Oxirredução
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Naphthoquinones); 0 (RNA, Small Interfering); 4707-32-8 (beta-lapachone); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (NQO1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190717


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[PMID]:29214656
[Au] Autor:Yang Y; Wang Y; Wang T; Jiang X; Wang L
[Ad] Endereço:Department of Clinical Pharmacy and Pharmacy Administration, West China School of Pharmacy, Sichuan University, Chengdu, China.
[Ti] Título:Screening active components of modified Xiaoyao powder as NRF2 agonists.
[So] Source:Cell Biochem Funct;35(8):518-526, 2017 Dec.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nuclear factor (erythroid-derived 2)-like 2 (NRF2) regulates antioxidant enzymes and phase II detoxifying enzymes, such as NAD(P)H: quinone oxidoreductase 1 (NQO1). Modified Xiaoyao powder (MXP) is most frequently used in the prevention and treatment of breast cancer in China. This study aimed to screen active components of MXP for antioxidant stress and chemoprevention, which depend on NRF2-NQO1 signalling pathway. A total of 25 monomeric compounds contained in MXP were screened using an antioxidant response element-luciferase reporter. The most potent antioxidant response element-luciferase inducers were chosen to further examine their effects on NRF2 and NQO1 in MCF-7 cells. These results were then confirmed by determining the oxidative stress levels and chemopreventive effect on inhibiting carcinogenesis transformation in NRF2 knockdown (NRF2 ) and NRF2 wild-type MCF-10A cells. We found that quercetin, kaempferol, and atractylenolide II in MXP were potent NRF2 inducers, which could up-regulate the expression of NRF2 and its downstream enzymes NQO1. In addition, these components could decrease reduced oxidative stress and inhibit carcinogenesis transformation, which depended on NRF2-NQO1 pathway. In conclusion, NRF2-NQO1 pathway plays an essential role in mediating the activity of MXP and its active components, at least in part; some beneficial effects of MXP may be applicable to breast cancer chemoprevention. Our study firstly found MXP active components including quercetin, kaempferol, and atractylenolide II. Our results firstly demonstrate that NRF2-NQO1 pathway plays an essential role in mediating the activity of MXP and its active components in breast cancer chemoprevention. Our study firstly found that atractylenolide II is a novel NRF2 inducer.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Neoplasias da Mama/prevenção & controle
Medicamentos de Ervas Chinesas/química
Fator 2 Relacionado a NF-E2/agonistas
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/isolamento & purificação
Células Cultivadas
Quimioprevenção
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Quempferóis/química
Quempferóis/isolamento & purificação
Quempferóis/farmacologia
Lactonas/química
Lactonas/isolamento & purificação
Lactonas/farmacologia
Estrutura Molecular
NAD(P)H Desidrogenase (Quinona)/antagonistas & inibidores
NAD(P)H Desidrogenase (Quinona)/genética
NAD(P)H Desidrogenase (Quinona)/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Extratos Vegetais/química
Extratos Vegetais/isolamento & purificação
Quercetina/química
Quercetina/isolamento & purificação
Quercetina/farmacologia
Sesquiterpenos/química
Sesquiterpenos/isolamento & purificação
Sesquiterpenos/farmacologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Drugs, Chinese Herbal); 0 (Kaempferols); 0 (Lactones); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (Plant Extracts); 0 (Sesquiterpenes); 0 (atractylenolide II); 0 (xiaoyao); 731P2LE49E (kaempferol); 9IKM0I5T1E (Quercetin); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (NQO1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3309


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[PMID]:29016672
[Au] Autor:Dai YC; Wang SC; Haque MM; Lin WH; Lin LC; Chen CH; Liu YW
[Ad] Endereço:Department of Microbiology, Immunology and Biopharmaceuticals, College of Life Sciences, National Chiayi University, Chiayi, Taiwan.
[Ti] Título:The interaction of arsenic and N-butyl-N-(4-hydroxybutyl)nitrosamine on urothelial carcinogenesis in mice.
[So] Source:PLoS One;12(10):e0186214, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The bladder is an important organ for the storage of excreted water and metabolites. If metabolites with carcinogenic characteristics are present in urine, the urothelial lining of the bladder could be damaged and genetically altered. In this study, we analyzed the interaction of arsenic and N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) on mouse bladder carcinogenesis. Our previous study found that arsenic affects BBN-altered urothelial enzymatic activity, protein expression, DNA oxidation and global DNA CpG methylation levels. In this study, two mouse models were used. First, after administering a co-treatment of BBN and arsenic for 20 weeks, BBN alone led to a urothelial carcinoma formation of 20%, and arsenic promoted a BBN-induced urothelial carcinoma formation of 10%. The protein expression of GSTM1, GSTO1, NQO1, and p21 did not change by arsenic along with the BBN co-treatment, but the Sp1 expression increased. In the second mouse model, BBN was a pretreatment promoter; arsenic dose-dependently deteriorated BBN-promoted dysplasia by 10% and 40% at 10 ppm and 100 ppm, respectively. Conversely, BBN pretreatment also accelerated arsenic-induced dysplasia by 30%. The urothelial carcinogenic effect reversed after ceasing BBN for a period of 20 weeks. In summary, three conclusions were drawn from this study. The first is the mutual promotion of arsenic and BBN in bladder carcinogenesis. Second, arsenic dosages without bladder carcinogenicity (10 ppm) or with slight carcinogenicity (100 ppm) promote BBN-induced mice bladder cancer progression. Finally, the dysplastic urothelium had reverted to near-normal morphology after ceasing BBN intake for 20 weeks, providing a good suggestion for people who want to quit smoking.
[Mh] Termos MeSH primário: Arsênico/toxicidade
Butilidroxibutilnitrosamina/toxicidade
Carcinogênese/induzido quimicamente
Carcinógenos/toxicidade
Carcinoma de Células de Transição/induzido quimicamente
Neoplasias da Bexiga Urinária/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Carcinogênese/metabolismo
Carcinogênese/patologia
Carcinoma de Células de Transição/genética
Carcinoma de Células de Transição/metabolismo
Carcinoma de Células de Transição/patologia
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Interações Medicamentosas
Feminino
Regulação Neoplásica da Expressão Gênica
Glutationa Transferase/genética
Glutationa Transferase/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
NAD(P)H Desidrogenase (Quinona)/genética
NAD(P)H Desidrogenase (Quinona)/metabolismo
Fator de Transcrição Sp1/agonistas
Fator de Transcrição Sp1/genética
Fator de Transcrição Sp1/metabolismo
Bexiga Urinária/efeitos dos fármacos
Bexiga Urinária/metabolismo
Bexiga Urinária/patologia
Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/metabolismo
Neoplasias da Bexiga Urinária/patologia
Urotélio/efeitos dos fármacos
Urotélio/metabolismo
Urotélio/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (Carrier Proteins); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Gsto1 protein, mouse); 0 (Sp1 Transcription Factor); 3817-11-6 (Butylhydroxybutylnitrosamine); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (Nqo1 protein, mouse); EC 2.5.1.18 (Glutathione Transferase); EC 2.5.1.18 (glutathione S-transferase M1); N712M78A8G (Arsenic)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186214


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[PMID]:28945821
[Au] Autor:Lee YS; Ku KM; Becker TM; Juvik JA
[Ad] Endereço:Department of Medical Biotechnology, Soonchunhyang University, Asan, South Korea.
[Ti] Título:Chemopreventive glucosinolate accumulation in various broccoli and collard tissues: Microfluidic-based targeted transcriptomics for by-product valorization.
[So] Source:PLoS One;12(9):e0185112, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Floret, leaf, and root tissues were harvested from broccoli and collard cultivars and extracted to determine their glucosinolate and hydrolysis product profiles using high performance liquid chromatography and gas chromotography. Quinone reductase inducing bioactivity, an estimate of anti-cancer chemopreventive potential, of the extracts was measured using a hepa1c1c7 murine cell line. Extracts from root tissues were significantly different from other tissues and contained high levels of gluconasturtiin and glucoerucin. Targeted gene expression analysis on glucosinolate biosynthesis revealed that broccoli root tissue has elevated gene expression of AOP2 and low expression of FMOGS-OX homologs, essentially the opposite of what was observed in broccoli florets, which accumulated high levels of glucoraphanin. Broccoli floret tissue has significantly higher nitrile formation (%) and epithionitrile specifier protein gene expression than other tissues. This study provides basic information of the glucosinolate metabolome and transcriptome for various tissues of Brassica oleracea that maybe utilized as potential byproducts for the nutraceutical market.
[Mh] Termos MeSH primário: Anticarcinógenos/metabolismo
Brassica/genética
Brassica/metabolismo
Glucosinolatos/genética
Glucosinolatos/metabolismo
[Mh] Termos MeSH secundário: Anticarcinógenos/análise
Brassica/química
Suplementos Nutricionais/análise
Topos Floridos/metabolismo
Perfilação da Expressão Gênica
Genes de Plantas
Glucose/análogos & derivados
Glucose/análise
Glucose/genética
Glucose/metabolismo
Glucosinolatos/análise
Seres Humanos
Hidrólise
Imidoésteres/análise
Imidoésteres/metabolismo
Metaboloma
Técnicas Analíticas Microfluídicas
NAD(P)H Desidrogenase (Quinona)/biossíntese
Folhas de Planta/metabolismo
Proteínas de Plantas/biossíntese
Raízes de Plantas/metabolismo
RNA de Plantas/genética
RNA de Plantas/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Glucosinolates); 0 (Imidoesters); 0 (Plant Proteins); 0 (RNA, Plant); 163ENC977A (gluconasturtiin); 21973-56-8 (glucoerucin); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185112


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[PMID]:28931237
[Au] Autor:Singh V; Prakhar P; Rajmani RS; Mahadik K; Borbora SM; Balaji KN
[Ad] Endereço:Department of Microbiology and Cell Biology, Indian Institute of Science.
[Ti] Título:Histone Methyltransferase SET8 Epigenetically Reprograms Host Immune Responses to Assist Mycobacterial Survival.
[So] Source:J Infect Dis;216(4):477-488, 2017 Aug 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NQO1 and TRXR1 are important host reductases implicated in the regulation of inflammation and apoptosis. Although the transcriptional machinery governing these processes have been extensively investigated, the associated epigenetic regulatory events remain unclear. Here, we report that SET8, a histone H4 lysine 20 monomethylase (H4K20me1), is highly induced during Mycobacterium tuberculosis infection that orchestrates immune evasion strategies through the induction of NQO1 and TRXR1 in vivo. SET8, along with FoxO3a, mediates an active NQO1-PGC1-α complex, which promotes the anti-inflammatory M2 macrophage phenotype, and assists TRXR1-regulated arrest of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis. Strikingly, the loss-of-function analysis in an in vivo mouse tuberculosis model further corroborated the pivotal role of SET8-responsive NQO1 and TRXR1 in mycobacterial survival. Thus, augmenting host immune responses against Mycobacterium tuberculosis by harnessing the SET8-NQO1/TRXR1 axis with its specific and potent inhibitors could lead to promising host-directed therapeutic adjuvants for tuberculosis treatment.
[Mh] Termos MeSH primário: Epigênese Genética
Histona-Lisina N-Metiltransferase/metabolismo
Interações Hospedeiro-Patógeno/genética
Interações Hospedeiro-Patógeno/imunologia
Mycobacterium tuberculosis/crescimento & desenvolvimento
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Modelos Animais de Doenças
Proteína Forkhead Box O3/genética
Proteína Forkhead Box O3/metabolismo
Regulação da Expressão Gênica
Histona-Lisina N-Metiltransferase/genética
Seres Humanos
Evasão da Resposta Imune
Leucócitos Mononucleares/microbiologia
Camundongos
NAD(P)H Desidrogenase (Quinona)/genética
NAD(P)H Desidrogenase (Quinona)/metabolismo
Células RAW 264.7
Reprodutibilidade dos Testes
Transdução de Sinais
Tiorredoxina Redutase 1/genética
Tiorredoxina Redutase 1/metabolismo
Tuberculose/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Box Protein O3); 0 (FoxO3 protein, mouse); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (Nqo1 protein, mouse); EC 1.8.1.9 (Thioredoxin Reductase 1); EC 1.8.1.9 (Txnrd1 protein, mouse); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (SET8 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix322


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[PMID]:28790194
[Au] Autor:Yonchuk JG; Foley JP; Bolognese BJ; Logan G; Wixted WE; Kou JP; Chalupowicz DG; Feldser HG; Sanchez Y; Nie H; Callahan JF; Kerns JK; Podolin PL
[Ad] Endereço:Stress and Repair Discovery Performance Unit, Respiratory Therapeutic Area, GlaxoSmithKline, King of Prussia, Pennsylvania.
[Ti] Título:Characterization of the Potent, Selective Nrf2 Activator, 3-(Pyridin-3-Ylsulfonyl)-5-(Trifluoromethyl)-2 -Chromen-2-One, in Cellular and In Vivo Models of Pulmonary Oxidative Stress.
[So] Source:J Pharmacol Exp Ther;363(1):114-125, 2017 Oct.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a key regulator of oxidative stress and cellular repair and can be activated through inhibition of its cytoplasmic repressor, Kelch-like ECH-associated protein 1 (Keap1). Several small molecule disrupters of the Nrf2-Keap1 complex have recently been tested and/or approved for human therapeutic use but lack either potency or selectivity. The main goal of our work was to develop a potent, selective activator of NRF2 as protection against oxidative stress. In human bronchial epithelial cells, our Nrf2 activator, 3-(pyridin-3-ylsulfonyl)-5-(trifluoromethyl)-2 -chromen-2-one (PSTC), induced Nrf2 nuclear translocation, Nrf2-regulated gene expression, and downstream signaling events, including induction of NAD(P)H:quinone oxidoreductase 1 (NQO1) enzyme activity and heme oxygenase-1 protein expression, in an Nrf2-dependent manner. As a marker of subsequent functional activity, PSTC restored oxidant ( -butyl hydroperoxide)-induced glutathione depletion. The compound's engagement of the Nrf2 signaling pathway translated to an in vivo setting, with induction of Nrf2-regulated gene expression and NQO1 enzyme activity, as well as restoration of oxidant (ozone)-induced glutathione depletion, occurring in the lungs of PSTC-treated rodents. Under disease conditions, PSTC engaged its target, inducing the expression of Nrf2-regulated genes in human bronchial epithelial cells derived from patients with chronic obstructive pulmonary disease, as well as in the lungs of cigarette smoke-exposed mice. Subsequent to the latter, a dose-dependent inhibition of cigarette smoke-induced pulmonary inflammation was observed. Finally, in contrast with bardoxolone methyl and sulforaphane, PSTC did not inhibit interleukin-1 -induced nuclear factor- B translocation or insulin-induced S6 phosphorylation in human cells, emphasizing the on-target activity of this compound. In summary, we characterize a potent, selective Nrf2 activator that offers protection against pulmonary oxidative stress in several cellular and in vivo models.
[Mh] Termos MeSH primário: Cumarínicos/uso terapêutico
Células Epiteliais/efeitos dos fármacos
Pulmão/efeitos dos fármacos
Fator 2 Relacionado a NF-E2/agonistas
Estresse Oxidativo/efeitos dos fármacos
Pneumonia/prevenção & controle
Doença Pulmonar Obstrutiva Crônica/metabolismo
Sulfonas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular
Núcleo Celular/metabolismo
Cumarínicos/administração & dosagem
Cumarínicos/sangue
Modelos Animais de Doenças
Descoberta de Drogas
Células Epiteliais/metabolismo
Expressão Gênica/efeitos dos fármacos
Glutationa/metabolismo
Células HEK293
Seres Humanos
Pulmão/metabolismo
Camundongos Endogâmicos C57BL
NAD(P)H Desidrogenase (Quinona)/genética
Fator 2 Relacionado a NF-E2/genética
Ozônio/toxicidade
Pneumonia/etiologia
Pneumonia/metabolismo
Transporte Proteico
RNA Interferente Pequeno/genética
Ratos Wistar
Fumar/efeitos adversos
Sulfonas/administração & dosagem
Sulfonas/sangue
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-(pyridin-3-ylsulfonyl)-5-(trifluoromethyl)-2H-chromen-2-one); 0 (Coumarins); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (RNA, Small Interfering); 0 (Sulfones); 66H7ZZK23N (Ozone); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.241794


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[PMID]:28780322
[Au] Autor:Niu L; Shao M; Liu Y; Hu J; Li R; Xie H; Zhou L; Shi L; Zhang R; Niu Y
[Ad] Endereço:Department of Toxicology, Hebei Medical University, Shijiazhuang, China; Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Jiankang Road 12, Shijiazhuang, 050011 Hebei, China.
[Ti] Título:Reduction of oxidative damages induced by titanium dioxide nanoparticles correlates with induction of the Nrf2 pathway by GSPE supplementation in mice.
[So] Source:Chem Biol Interact;275:133-144, 2017 Sep 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Titanium dioxide nanoparticles (TiO NPs) are widely used to additives in cosmetics, pharmaceuticals, paints and foods. Recent studies have demonstrated that TiO NPs increased the risk of cancer and the mechanism might relate with oxidative stress. Grape seed procyanidin extract (GSPE) is a natural compound which has been demonstrated to possess a wide array of pharmacological and biochemical actions, including anti-inflammatory, anti-carcinogenic, and antioxidant properties. Our data show that GSPE prevents the changes of histopathology and biomarkers in heart, liver and kidney that occur in mice exposed to TiO NPs. After pretreatment with GSPE, the DNA damage, reactive oxygen species (ROS) generation and malondialdehyde (MDA) content in mice exposed to TiO NPs had statistically significant decreases in dose dependent manners. GSPE increased the expression of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), NAD(P)H dehydrogenase[quinine] 1(NQO1), heme oxygenase 1 (HO-1) and glutamate-cysteine ligase catalytic subunit (GCLC). We conclude that grape seed procyanidin extract prevents the majority of tissue and molecular damage resulting from nanoparticle treatment. The protective effect of GSPE may be due to its strong antioxidative activities which related with the activated Nrf2 and its down-regulated genes including NQO1, HO-1 and GCLC.
[Mh] Termos MeSH primário: Suplementos Nutricionais
Extrato de Sementes de Uva
Nanopartículas Metálicas/toxicidade
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/fisiologia
Titânio/química
[Mh] Termos MeSH secundário: Animais
Biflavonoides/química
Biflavonoides/isolamento & purificação
Biflavonoides/farmacologia
Catequina/química
Catequina/isolamento & purificação
Catequina/farmacologia
Dano ao DNA/efeitos dos fármacos
Regulação para Baixo/efeitos dos fármacos
Glutamato-Cisteína Ligase/metabolismo
Extrato de Sementes de Uva/química
Heme Oxigenase-1/metabolismo
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Malondialdeído/metabolismo
Nanopartículas Metálicas/química
Camundongos
NAD(P)H Desidrogenase (Quinona)/metabolismo
Proantocianidinas/química
Proantocianidinas/isolamento & purificação
Proantocianidinas/farmacologia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biflavonoids); 0 (Grape Seed Extract); 0 (NF-E2-Related Factor 2); 0 (Proanthocyanidins); 0 (Reactive Oxygen Species); 15FIX9V2JP (titanium dioxide); 4852-22-6 (procyanidin); 4Y8F71G49Q (Malondialdehyde); 8R1V1STN48 (Catechin); D1JT611TNE (Titanium); 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 6.3.2.2 (Glutamate-Cysteine Ligase)
[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:170807
[St] Status:MEDLINE


  8 / 3540 MEDLINE  
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[PMID]:28771686
[Au] Autor:Muñoz IG; Morel B; Medina-Carmona E; Pey AL
[Ad] Endereço:Crystallography and Protein Engineering Unit, Structural Biology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
[Ti] Título:A mechanism for cancer-associated inactivation of NQO1 due to P187S and its reactivation by the consensus mutation H80R.
[So] Source:FEBS Lett;591(18):2826-2835, 2017 Sep.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The cancer-associated P187S polymorphism in the NAD(P)H:quinone oxidoreductase 1 (NQO1) abolishes enzyme activity by strongly reducing FAD binding affinity. A single mammalian consensus mutation (H80R) protects P187S from inactivation. To provide mechanistic insight into these effects, we report here a detailed structural and thermodynamic characterization of FAD binding to these NQO1 variants. Our results show that H80R causes a population shift in the conformational ensemble of apo-P187S, remodelling the structure and dynamics of the FAD-binding site and reducing the energetic penalization arising from the equilibrium between apo- and holo-states. Our analyses illustrate how single amino acid changes can profoundly affect structural and mechanistic features of protein functional traits, with implications for our understanding of protein evolution and human disease.
[Mh] Termos MeSH primário: NAD(P)H Desidrogenase (Quinona)/química
NAD(P)H Desidrogenase (Quinona)/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Calorimetria
Escherichia coli
Predisposição Genética para Doença/genética
Seres Humanos
Mutação
NAD(P)H Desidrogenase (Quinona)/genética
Neoplasias/genética
Polimorfismo de Nucleotídeo Único/genética
Ligação Proteica
Estrutura Secundária de Proteína
Espectroscopia de Infravermelho com Transformada de Fourier
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (NQO1 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12772


  9 / 3540 MEDLINE  
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[PMID]:28710963
[Au] Autor:Zhang X; Bian J; Li X; Wu X; Dong Y; You Q
[Ad] Endereço:State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China; Department of Organic Chemistry, School of Science, China Pharmaceutical University, Nanjing 211198, China.
[Ti] Título:2-Substituted 3,7,8-trimethylnaphtho[1,2-b]furan-4,5-diones as specific L-shaped NQO1-mediated redox modulators for the treatment of non-small cell lung cancer.
[So] Source:Eur J Med Chem;138:616-629, 2017 Sep 29.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Based on the scaffold of 3,7,8-trimethylnaphtho[1,2-b]furan-4,5-dione, a series of L-shaped derivatives with substituted side chains at the position of C2 were designed by analyzing the binding mode with NQO1. The drug-like compound 6q (named as DDO-7178) emerged as the most specific substrate of the two-electron oxidoreductase NQO1 and could hardly be reduced by one-electron oxidoreductases CPR (NQO1/CPR = 20.8). In addition, compound 6q showed much improved physicochemical properties such as water solubility than the control ß-lap. The follow-up studies indicated that 6q showed a NQO1-expressing cancer-cell-selective killing property. Preliminary mechanism studies on the anticancer effect indicated that 6q induced ROS production in an NQO1 dependent manner and activated Akt/MAPK pathways in a ROS-dependent fashion, thereby inducing apoptosis. In addition, emphasized compound 6q showed more significant antitumor efficacy than ß-lap without producing obvious toxic effects in vivo, which gave us a new tool for further investigation of NQO1-mediated redox modulators as anticancer drugs for the treatment of NQO1-overexpressed NSCLC.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Furanos/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
NAD(P)H Desidrogenase (Quinona)/metabolismo
Naftalenos/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Carcinoma Pulmonar de Células não Pequenas/patologia
Morte Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Furanos/síntese química
Furanos/química
Seres Humanos
Neoplasias Pulmonares/patologia
Modelos Moleculares
Estrutura Molecular
Naftalenos/síntese química
Naftalenos/química
Oxirredução
Espécies Reativas de Oxigênio/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,7,8-trimethylnaphtho(1,2-b)furan-4,5-dione); 0 (Antineoplastic Agents); 0 (Furans); 0 (Naphthalenes); 0 (Reactive Oxygen Species); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (NQO1 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


  10 / 3540 MEDLINE  
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[PMID]:28655519
[Au] Autor:Qi X; Qin Z; Tang J; Han P; Xing Q; Wang K; Yu J; Zhou G; Tang M; Wang W; Zhang W
[Ad] Endereço:Department of Urology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China; Department of Urology, Subei People's Hospital, Yangzhou 225000, China.
[Ti] Título:Omega-3 polyunsaturated fatty acids ameliorates testicular ischemia-reperfusion injury through the induction of Nrf2 and inhibition of NF-κB in rats.
[So] Source:Exp Mol Pathol;103(1):44-50, 2017 Aug.
[Is] ISSN:1096-0945
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study was designed to investigate the protective effect of Omega-3 polyunsaturated fatty acids (n-3 PUFAs) on testicular ischemia-reperfusion (I/R) injury in rats. METHODS: A total of 24 rats were randomly divided into the following three groups: Group A (Control group, n=8), Group B (I/R group, n=8), Group C (I/R group treated with n-3 PUFAs, n=8). Histological examination was used to assess changes in testicular structure. Tissue oxidative stress biomarkers, malondialdehyde (MDA) as well as Superoxide, and antioxidant indexes, including total antioxidant capacity (T-AOC); catalase (CAT); glutathione (GSH); glutathione/glutathione disulfide ratio (GSH/GSSG); superoxide dismutase (SOD) were determined. In addition, nuclear transcription factor erythroid 2-related factor 2 (Nrf2), Nrf2-dependent antioxidant enzymes, such as heme oxygenase-1 (HO-1) and NADPH quinine oxidoreductase-1 (NQO-1), and nuclear factor kappa B (NF-κB) were detected. RESULTS: Compared to I/R group, n-3 PUFAs could obviously increase the mean seminiferous tubular diameter in the histological examination. After n-3 PUFAs treatment, the level of tissue MDA and Superoxide were significantly decreased, while tissue T-AOC, CAT, GSH, GSH/GSSG and SOD levels were significantly increased, compared to I/R group (P<0.05). Besides, the expression levels of Nrf2, HO-1, and NQO-1 were significantly higher and the NF-κB expression level was significantly lower in the n-3 PUFAs treated group than that in I/R group (P<0.05). CONCLUSIONS: These results provided evidences that n-3 PUFAs ameliorated testes damage caused by testicular I/R injury through its antioxidative capacity and anti-inflammatory effects, involving the activation of Nrf2 and the inhibition of NF-κB.
[Mh] Termos MeSH primário: Ácidos Graxos Ômega-3/farmacologia
Fator 2 Relacionado a NF-E2/metabolismo
NF-kappa B/metabolismo
Traumatismo por Reperfusão/tratamento farmacológico
Testículo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Regulação da Expressão Gênica
Glutationa/metabolismo
Heme Oxigenase-1/genética
Heme Oxigenase-1/metabolismo
Masculino
Malondialdeído/sangue
NAD(P)H Desidrogenase (Quinona)/genética
NAD(P)H Desidrogenase (Quinona)/metabolismo
Fator 2 Relacionado a NF-E2/genética
NF-kappa B/genética
Estresse Oxidativo/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fatty Acids, Omega-3); 0 (NF-E2-Related Factor 2); 0 (NF-kappa B); 0 (Nfe2l2 protein, rat); 4Y8F71G49Q (Malondialdehyde); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.15.1.1 (Superoxide Dismutase); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (NQO1 protein, rat); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE



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