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Pesquisa : D01.857 [Categoria DeCS]
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[PMID]:28271743
[Au] Autor:Wu H; Sun L; Wang H; Wang X
[Ad] Endereço:a Key Laboratory of Regional Environment and Eco-Remediation , Ministry of Education, Shenyang University , Shenyang , People's Republic of China.
[Ti] Título:In situ sodium persulfate/calcium peroxide oxidation in remediation of TPH-contaminated soil in 3D-sand box.
[So] Source:Environ Technol;39(1):91-101, 2018 Jan.
[Is] ISSN:0959-3330
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this article was to obtain the application parameters and conditions of in situ sodium persulfate/calcium peroxide oxidation. For the purposes of remediation, soil from a total petroleum hydrocarbons (TPH)-contaminated site was collected and prepared to reflect the actual stratum condition in a newly developed soil remediation modeling apparatus. Application methods of soil mixture, natural infiltration, direct injection and groundwater circulation were used to simulate in situ sodium persulfate oxidation in TPH-contaminated soil. Results showed that the transfer capability of Na S O in simulated soil was strong Na S O migrated to the saturated layer after 3 days of in situ injection, which then continued both horizontal and vertical migration. After 7 days the oxidant was widespread in the saturated layer with a radius of influence of 0.4 m. It was found that mixing CaO /Fe /CA with soil and spraying Na S O can effectively repair the surface-contaminated soil, and the longitudinal migration of Na S O in the reaction process can further strengthen the remediation of the upper layer soil. Due to the buffering effect of the soil, the effect of oxidation on the pH and temperature of different soil layers was small, but detectable in comparison to natural environmental factors.
[Mh] Termos MeSH primário: Recuperação e Remediação Ambiental/métodos
Hidrocarbonetos/química
Peróxidos/química
Poluição por Petróleo/análise
Petróleo/análise
Poluentes do Solo/análise
[Mh] Termos MeSH secundário: Oxirredução
Petróleo/metabolismo
Compostos de Sódio
Poluentes do Solo/química
Sulfatos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydrocarbons); 0 (Peroxides); 0 (Petroleum); 0 (Sodium Compounds); 0 (Soil Pollutants); 0 (Sulfates); 7FRO2ENO91 (calcium peroxide); J49FYF16JE (sodium persulfate)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE
[do] DOI:10.1080/09593330.2017.1296029


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[PMID]:28469096
[Au] Autor:Wang XN; Zhang CJ; Diao HL; Zhang Y
[Ad] Endereço:Reproductive Medical Center of Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, China.
[Ti] Título:Protective Effects of Curcumin against Sodium Arsenite-induced Ovarian Oxidative Injury in a Mouse Model.
[So] Source:Chin Med J (Engl);130(9):1026-1032, 2017 May 05.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Excessive reactive oxygen species (ROS) may lead to a number of reproductive diseases such as polycystic ovary syndrome. This study aimed to establish an animal model of ovarian oxidative stress and to assess the protective effect of curcumin against oxidative injury. METHODS: Ovarian oxidative stress was induced in female Kunming mice (n = 40) with intraperitoneal injection of 8 mg/kg sodium arsenite (As) once every other day for 16 days; meanwhile, they were, respectively, treated by intragastric administration of 0, 100, 150, or 200 mg/kg (n = 10/group) curcumin once per day for 21 days. Ten normal mice were used as control. Then, the mice were injected intraperitoneally with BrdU and sacrificed; the right ovaries were collected for hematoxylin and eosin (HE) staining and BrdU immunohistochemistry, and the left ovaries for enzyme-linked immunosorbent assay (ELISA) and Western blotting analyses. RESULTS: The ELISA results showed that ROS (11.74 ± 0.65 IU/mg in 8 mg/kg AS + 0 mg/kg curcumin group vs. 10.71 ± 0.91 IU/mg in control group, P= 0.021) and malondialdehyde (MDA) (0.32 ± 0.02 nmol/g in 8 mg/kg AS + 0 mg/kg curcumin group vs. 0.27 ± 0.02 nmol/g in control group, P= 0.048) increased while superoxide dismutase (SOD) (3.96 ± 0.36 U/mg in 8 mg/kg AS + 0 mg/kg curcumin group vs. 4.51 ± 0.70 U/mg in control group, P= 0.012) and glutathione peroxidase (17.36 ± 1.63 U/g in 8 mg/kg AS + 0 mg/kg curcumin group vs. 18.92 ± 1.80 U/g in control group, P= 0.045) decreased in the ovary after injection of As, indicating successful modeling of oxidative stress. Curcumin treatment could considerably increase SOD (4.57 ± 0.68, 4.49 ± 0.27, and 4.56 ± 0.25 U/mg in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, allP < 0.05) while significantly reduce ROS (10.64 ± 1.38, 10.73 ± 0.71, and 10.67 ± 1.38 IU/mg in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, allP < 0.05) and MDA (0.28 ± 0.02, 0.25 ± 0.03, and 0.27 ± 0.04 nmol/g in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively; bothP < 0.05) in the ovary. HE staining and BrdU immunohistochemistry of the ovarian tissues indicated the increased amount of atretic follicles (5.67 ± 0.81, 5.84 ± 0.98, and 5.72 ± 0.84 in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, all P < 0.05), and the inhibited proliferation of granular cells under oxidative stress would be reversed by curcumin. Furthermore, the Western blotting of ovarian tissues showed that the p66Shc expression upregulated under oxidative stress would be lowered by curcumin. CONCLUSION: Curcumin could alleviate arsenic-induced ovarian oxidative injury to a certain extent.
[Mh] Termos MeSH primário: Arsenitos/toxicidade
Curcumina/uso terapêutico
Compostos de Sódio/toxicidade
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Feminino
Glutationa Peroxidase/metabolismo
Imuno-Histoquímica
Malondialdeído/metabolismo
Camundongos
Ovário/efeitos dos fármacos
Ovário/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Síndrome do Ovário Policístico/tratamento farmacológico
Síndrome do Ovário Policístico/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenites); 0 (Reactive Oxygen Species); 0 (Sodium Compounds); 48OVY2OC72 (sodium arsenite); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.204927


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[PMID]:28873450
[Au] Autor:Yokota T; Omachi K; Suico MA; Kojima H; Kamura M; Teramoto K; Kaseda S; Kuwazuru J; Shuto T; Kai H
[Ad] Endereço:Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Chuo-ku, Kumamoto City, Kumamoto, Japan.
[Ti] Título:Bromide supplementation exacerbated the renal dysfunction, injury and fibrosis in a mouse model of Alport syndrome.
[So] Source:PLoS One;12(9):e0183959, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A seminal study recently demonstrated that bromide (Br-) has a critical function in the assembly of type IV collagen in basement membrane (BM), and suggested that Br- supplementation has therapeutic potential for BM diseases. Because salts of bromide (KBr and NaBr) have been used as antiepileptic drugs for several decades, repositioning of Br- for BM diseases is probable. However, the effects of Br- on glomerular basement membrane (GBM) disease such as Alport syndrome (AS) and its impact on the kidney are still unknown. In this study, we administered daily for 16 weeks 75 mg/kg or 250 mg/kg (within clinical dosage) NaBr or NaCl (control) via drinking water to 6-week-old AS mice (mouse model of X-linked AS). Treatment with 75 mg/kg NaBr had no effect on AS progression. Surprisingly, compared with 250 mg/kg NaCl, 250 mg/kg NaBr exacerbated the progressive proteinuria and increased the serum creatinine and blood urea nitrogen in AS mice. Histological analysis revealed that glomerular injury, renal inflammation and fibrosis were exacerbated in mice treated with 250 mg/kg NaBr compared with NaCl. The expressions of renal injury markers (Lcn2, Lysozyme), matrix metalloproteinase (Mmp-12), pro-inflammatory cytokines (Il-6, Il-8, Tnf-α, Il-1ß) and pro-fibrotic genes (Tgf-ß, Col1a1, α-Sma) were also exacerbated by 250 mg/kg NaBr treatment. Notably, the exacerbating effects of Br- were not observed in wild-type mice. These findings suggest that Br- supplementation needs to be carefully evaluated for real positive health benefits and for the absence of adverse side effects especially in GBM diseases such as AS.
[Mh] Termos MeSH primário: Brometos/efeitos adversos
Nefropatias/metabolismo
Cirrose Hepática
Nefrite Hereditária/metabolismo
[Mh] Termos MeSH secundário: Animais
Nitrogênio da Ureia Sanguínea
Brometos/farmacologia
Creatinina/sangue
Modelos Animais de Doenças
Membrana Basal Glomerular/patologia
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Nefrite/patologia
Nitrogênio/sangue
Compostos de Potássio/efeitos adversos
Compostos de Potássio/farmacologia
Proteinúria/metabolismo
Compostos de Sódio/efeitos adversos
Compostos de Sódio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bromides); 0 (Potassium Compounds); 0 (Sodium Compounds); AYI8EX34EU (Creatinine); LC1V549NOM (sodium bromide); N762921K75 (Nitrogen); OSD78555ZM (potassium bromide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183959


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[PMID]:28843991
[Au] Autor:Li J; Zhao L; Zhang Y; Li W; Duan X; Chen J; Guo Y; Yang S; Sun G; Li B
[Ad] Endereço:Environment and Non-Communicable Disease Research Center, Key Laboratory of Arsenic-related Biological Effects and Prevention and Treatment in Liaoning Province, School of Public Health, China Medical University, Shenyang 110122, China; Department of Occupational and Environmental Health, Key Labora
[Ti] Título:Imbalanced immune responses involving inflammatory molecules and immune-related pathways in the lung of acute and subchronic arsenic-exposed mice.
[So] Source:Environ Res;159:381-393, 2017 11.
[Is] ISSN:1096-0953
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Inorganic arsenic has been claimed to increase the risk of pulmonary diseases through ingestion, as opposed to inhalation, which makes it a unique and intriguing environmental toxicant. However, the immunotoxic effects of lung, one of the targets of arsenic exposure, have not been extensively investigated in vivo. In the present study, we first confirmed that 2.5, 5 and 10mg/kg NaAsO orally for 24h dose-dependently triggered the infiltration of neutrophils, lymphocytes and macrophages in BALF. Not only the transcription activity, but also the secretion of proinflammatory cytokines IL-1ß, IL-6 and TNF-α were consistently raised in the lung and BALF of acute arsenic-exposed mice. Acute oral administration of NaAsO also raised pulmonary MPO activity and mRNA levels of chemokine Mip-2 and Mcp-1. Meanwhile, obvious histopathological damages with inflammatory cells infiltration and erythrocyte aggregation around the capillaries were verified in the lung of mice drank arsenic-rich water freely for 3 months. Furthermore, we affirmed notable disturbance of CD4 T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-γ of Th1, as well as lessened Ror-γt and Il-23 of Th17. However, impressive elevation of cytokine Ifn-γ and Il-23, as well as moderate enhancement of Il-4 and Il-10 were found in the lung by subchronic arsenic administration. Finally, our present study demonstrated that both a single and sustained arsenic exposure prominently increased the expression of immune-related p38, JNK, ERK1/2 and NF-κB proteins in the lung tissue. While disrupting the pulmonary redox homeostasis by increasing MDA levels, exhausting GSH and impaired enzyme activities of CAT and GSH-Px, antioxidant regulator NRF2 and its downstream targets HO-1 and GSTO1/2 were also up-regulated by both acute and subchronic arsenic treatment. Conclusively, our present study demonstrated both acute and subchronic oral administration of arsenic triggers multiple pulmonary immune responses involving inflammatory molecules and T-cell differentiation, which might be closely associated with the imbalanced redox status and activation of immune-related MAPKs, NF-κB and anti-inflammatory NRF2 pathways.
[Mh] Termos MeSH primário: Arsênico/toxicidade
Arsenitos/toxicidade
Poluentes Ambientais/toxicidade
Compostos de Sódio/toxicidade
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Diferenciação Celular/efeitos dos fármacos
Citocinas/efeitos dos fármacos
Citocinas/imunologia
Relação Dose-Resposta a Droga
Feminino
Pulmão/efeitos dos fármacos
Pulmão/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Testes de Toxicidade Aguda
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arsenites); 0 (Cytokines); 0 (Environmental Pollutants); 0 (Sodium Compounds); 48OVY2OC72 (sodium arsenite); N712M78A8G (Arsenic)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170828
[St] Status:MEDLINE


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[PMID]:28750289
[Au] Autor:Outsiou A; Frontistis Z; Ribeiro RS; Antonopoulou M; Konstantinou IK; Silva AMT; Faria JL; Gomes HT; Mantzavinos D
[Ad] Endereço:Department of Chemical Engineering, University of Patras, Caratheodory 1, University Campus, GR-26504 Patras, Greece.
[Ti] Título:Activation of sodium persulfate by magnetic carbon xerogels (CX/CoFe) for the oxidation of bisphenol A: Process variables effects, matrix effects and reaction pathways.
[So] Source:Water Res;124:97-107, 2017 Nov 01.
[Is] ISSN:1879-2448
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An advanced oxidation process comprising sodium persulfate (SPS) and a novel magnetic carbon xerogel was tested for the degradation of bisphenol A (BPA), a model endocrine-disrupting compound. The catalyst, consisting of interconnected carbon microspheres with embedded iron and cobalt microparticles, was capable of activating persulfate to form sulfate and hydroxyl radicals at ambient conditions. The pseudo-first order degradation rate of BPA in ultrapure water (UPW) was found to increase with (i) increasing catalyst (25-75 mg/L) and SPS (31-250 mg/L) concentrations, (ii) decreasing BPA concentration (285-14,200 µg/L), and (iii) changing pH from alkaline to acidic values (9-3). Besides UPW, tests were conducted in drinking water, treated wastewater, groundwater and surface water; interestingly, the rate in UPW was always lower than in any other matrix containing several organic and inorganic constituents. The effect of natural organic matter (in the form of humic acids) and alcohols was detrimental to BPA degradation owing to the scavenging of radicals. Conversely, chlorides at concentrations greater than 50 mg/L had a positive effect due to the formation and subsequent participation of chlorine-containing radicals. Liquid chromatography time-of-flight mass spectrometry was employed to identify major transformation by-products (TBPs) of BPA degradation in the absence and presence of chlorides; in the latter case, several chlorinated TBPs were detected confirming the role of Cl-related radicals. Based on TBPs, main reaction pathways are proposed.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/química
Fenóis/química
Poluentes Químicos da Água/química
[Mh] Termos MeSH secundário: Carbono
Oxirredução
Compostos de Sódio
Sulfatos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Phenols); 0 (Sodium Compounds); 0 (Sulfates); 0 (Water Pollutants, Chemical); 7440-44-0 (Carbon); J49FYF16JE (sodium persulfate); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE


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[PMID]:28602540
[Au] Autor:Luz AL; Godebo TR; Smith LL; Leuthner TC; Maurer LL; Meyer JN
[Ad] Endereço:Nicholas School of the Environment, Box 90328, Duke University, Durham, NC, 27708, USA.
[Ti] Título:Deficiencies in mitochondrial dynamics sensitize Caenorhabditis elegans to arsenite and other mitochondrial toxicants by reducing mitochondrial adaptability.
[So] Source:Toxicology;387:81-94, 2017 Jul 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Mitochondrial fission, fusion, and mitophagy are interlinked processes that regulate mitochondrial shape, number, and size, as well as metabolic activity and stress response. The fundamental importance of these processes is evident in the fact that mutations in fission (DRP1), fusion (MFN2, OPA1), and mitophagy (PINK1, PARK2) genes can cause human disease (collectively >1/10,000). Interestingly, however, the age of onset and severity of clinical manifestations varies greatly between patients with these diseases (even those harboring identical mutations), suggesting a role for environmental factors in the development and progression of certain mitochondrial diseases. Using the model organism Caenorhabditis elegans, we screened ten mitochondrial toxicants (2, 4-dinitrophenol, acetaldehyde, acrolein, aflatoxin B , arsenite, cadmium, cisplatin, doxycycline, paraquat, rotenone) for increased or decreased toxicity in fusion (fzo-1, eat-3)-, fission (drp-1)-, and mitophagy (pdr-1, pink-1)-deficient nematodes using a larval growth assay. In general, fusion-deficient nematodes were the most sensitive to toxicants, including aflatoxin B , arsenite, cisplatin, paraquat, and rotenone. Because arsenite was particularly potent in fission- and fusion-deficient nematodes, and hundreds of millions of people are chronically exposed to arsenic, we investigated the effects of these genetic deficiencies on arsenic toxicity in more depth. We found that deficiencies in fission and fusion sensitized nematodes to arsenite-induced lethality throughout aging. Furthermore, low-dose arsenite, which acted in a "mitohormetic" fashion by increasing mitochondrial function (in particular, basal and maximal oxygen consumption) in wild-type nematodes by a wide range of measures, exacerbated mitochondrial dysfunction in fusion-deficient nematodes. Analysis of multiple mechanistic changes suggested that disruption of pyruvate metabolism and Krebs cycle activity underlie the observed arsenite-induced mitochondrial deficits, and these disruptions are exacerbated in the absence of mitochondrial fusion. This research demonstrates the importance of mitochondrial dynamics in limiting arsenite toxicity by permitting mitochondrial adaptability. It also suggests that individuals suffering from deficiencies in mitodynamic processes may be more susceptible to the mitochondrial toxicity of arsenic and other toxicants.
[Mh] Termos MeSH primário: Arsenitos/toxicidade
Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Dinâmica Mitocondrial/efeitos dos fármacos
Compostos de Sódio/toxicidade
[Mh] Termos MeSH secundário: Animais
Autofagia/efeitos dos fármacos
Caenorhabditis elegans/embriologia
Caenorhabditis elegans/genética
Caenorhabditis elegans/metabolismo
Proteínas de Caenorhabditis elegans/genética
Relação Dose-Resposta a Droga
Dinaminas/genética
Dinaminas/metabolismo
GTP Fosfo-Hidrolases/genética
GTP Fosfo-Hidrolases/metabolismo
Interação Gene-Ambiente
Genótipo
Larva/efeitos dos fármacos
Larva/metabolismo
Mitocôndrias/metabolismo
Degradação Mitocondrial/efeitos dos fármacos
Fenótipo
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenites); 0 (Caenorhabditis elegans Proteins); 0 (Sodium Compounds); 48OVY2OC72 (sodium arsenite); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (parkin protein); EC 2.7.11.1 (PINK1 protein, C elegans); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.6.1.- (EAT-3 protein, C elegans); EC 3.6.1.- (FZO-1 protein, C elegans); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.5.5 (Dynamins); EC 3.6.5.5 (dynamin-related protein 1, C elegans)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


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[PMID]:28556958
[Au] Autor:Kim Y; Park SE; Moon JW; Kim BM; Kim HG; Jeong IG; Yoo S; Ahn JB; You D; Pak JH; Kim S; Hwang JJ; Kim CS
[Ad] Endereço:Department of Urology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
[Ti] Título:Downregulation of androgen receptors by NaAsO via inhibition of AKT-NF-κB and HSP90 in castration resistant prostate cancer.
[So] Source:Prostate;77(10):1128-1136, 2017 Jul.
[Is] ISSN:1097-0045
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Androgen and androgen receptor (AR) play essential roles in the development and maintenance of prostate cancer. The recently identified AR splice variants (AR-Vs) have been considered as a plausible mechanism for the primary resistance against androgen deprivation therapy (ADT) in castration-resistant prostate cancer (CRPC). Sodium meta-arsenite (NaAsO ; KML001; Kominox), a trivalent arsenical, is an orally bioavailable and water soluble, which is currently in phase I/II clinical trials for the treatment of prostate cancer. It has a potent anti-cancer effect on prostate cancer cells and xenografts. The aim of this study was to examine the effect of NaAsO on AR signaling in LNCaP and 22Rv1 CRPC cells. METHODS: We used hormone-sensitive LNCaP cells, hormone-insensitive 22Rv1 cells, and CRPC patient-derived primary cells. We analyzed anti-cancer effect of NaAsO using real-time quantitative reverse transcription-PCR, Western blotting, immunofluorescence staining and CellTiter Glo® luminescent assay. Statistical evaluation of the results was performed by one-way ANOVA. RESULTS: NaAsO significantly reduced the translocation of AR and AR-Vs to the nucleus as well as their level in LNCaP and 22Rv1 cells. Besides, the level of the prostate-specific antigen (PSA), downstream target gene of AR, was also decreased. This compound was also an effective modulator of AKT-dependent NF-κB activation which regulates AR. NaAsO significantly inhibited phosphorylation of AKT and expression and nuclear translocation of NF-κB. We then investigated the effect of NaAsO on AR stabilization. NaAsO promoted HSP90 acetylation by down-regulating HDAC6, which reduces the stability of AR in prostate cancer cells. CONCLUSIONS: Here, we show that NaAsO disrupts AR signaling at multiple levels by affecting AR expression, stability, and degradation in primary tumor cell cultures from prostate cancer patients as well as CRPC cell lines. These results suggest that NaAsO could be a novel therapeutics for prostate cancer.
[Mh] Termos MeSH primário: Arsenitos/farmacologia
Próstata
Neoplasias de Próstata Resistentes à Castração
Receptores Androgênicos/metabolismo
Transdução de Sinais/efeitos dos fármacos
Compostos de Sódio/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação para Baixo
Inibidores Enzimáticos/farmacologia
Proteínas de Choque Térmico HSP90/metabolismo
Seres Humanos
Masculino
NF-kappa B/metabolismo
Próstata/efeitos dos fármacos
Próstata/metabolismo
Próstata/patologia
Antígeno Prostático Específico/análise
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Neoplasias de Próstata Resistentes à Castração/metabolismo
Neoplasias de Próstata Resistentes à Castração/patologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenites); 0 (Enzyme Inhibitors); 0 (HSP90 Heat-Shock Proteins); 0 (NF-kappa B); 0 (Receptors, Androgen); 0 (Sodium Compounds); 48OVY2OC72 (sodium arsenite); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.21.77 (Prostate-Specific Antigen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1002/pros.23370


  8 / 2309 MEDLINE  
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[PMID]:28549828
[Au] Autor:Cui Q; Fu J; Hu Y; Li Y; Yang B; Li L; Sun J; Chen C; Sun G; Xu Y; Zhang Q; Pi J
[Ad] Endereço:Program of Environmental Toxicology, School of Public Health, China Medical University, No 77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, PR China.
[Ti] Título:Deficiency of long isoforms of Nfe2l1 sensitizes MIN6 pancreatic ß cells to arsenite-induced cytotoxicity.
[So] Source:Toxicol Appl Pharmacol;329:67-74, 2017 Aug 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increasing evidence indicates that chronic inorganic arsenic exposure is associated with type 2 diabetes (T2D), a disease of growing prevalence. Pancreatic ß-cells were targeted and damaged by oxidative stress induced by arsenite. We previously showed that nuclear factor erythroid 2 like 2 (Nfe2l2)-deficient pancreatic ß-cells were vulnerable to cell damage induced by oxidative stressors including arsenite, due to a muted antioxidant response. Like nuclear factor erythroid 2 like 2 (NFE2L2), NFE2L1 also belongs to the cap 'n' collar (CNC) basic-region leucine zipper (bZIP) transcription factor family, and regulates antioxidant response element (ARE) related genes. Our prior work showed NFE2L1 regulates glucose-stimulated insulin secretion (GSIS) in pancreatic ß-cells and isolated islets. In the current study, we demonstrated that MIN6 cells with a specific knockdown of long isoforms of Nfe2l1 (L-Nfe2l1) by lentiviral shRNA (Nfe2l1(L)-KD) were vulnerable to arsenite-induced apoptosis and cell damage. The expression levels of antioxidant genes, such as Gclc, Gclm and Ho-1, and intracellular reactive oxygen species (ROS) levels were not different in Scramble and Nfe2l1(L)-KD cells, while the expression of arsenic metabolism related-genes, such as Gsto1, Gstm1 and Nqo1, increased in Nfe2l1(L)-KD cells with or without arsenite treatment. The up-regulation of arsenic biotransformation genes was due to activated NFE2L2 in Nfe2l1(L)-KD MIN6 cells. Furthermore, the level of intracellular monomethylarsenic (MMA) was higher in Nfe2l1(L)-KD MIN6 cells than in Scramble cells. These results showed that deficiency of L-Nfe2l1 in pancreatic ß-cells increased susceptibility to acute arsenite-induced cytotoxicity by promoting arsenic biotransformation and intracellular MMA levels.
[Mh] Termos MeSH primário: Arsenitos/toxicidade
Células Secretoras de Insulina/efeitos dos fármacos
Fator 1 Relacionado a NF-E2/deficiência
Compostos de Sódio/toxicidade
[Mh] Termos MeSH secundário: Animais
Arsenitos/metabolismo
Biotransformação/genética
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica
Células Secretoras de Insulina/enzimologia
Células Secretoras de Insulina/patologia
Metilação
Camundongos
Fator 1 Relacionado a NF-E2/genética
Estresse Oxidativo/efeitos dos fármacos
Isoformas de Proteínas
Interferência de RNA
RNA Mensageiro/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Compostos de Sódio/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenites); 0 (NF-E2-Related Factor 1); 0 (Nfe2L1 protein, mouse); 0 (Protein Isoforms); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 0 (Sodium Compounds); 48OVY2OC72 (sodium arsenite)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE


  9 / 2309 MEDLINE  
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[PMID]:28530560
[Au] Autor:Wang M; Gasmalla MAA; Admassu Tessema H; Hua X; Yang R
[Ad] Endereço:State Key Laboratory of Food Science and Technology, Jiangnan University, 214122 Wuxi, China; School of Food Science and Technology, Jiangnan University, 214122 Wuxi, China. Electronic address: wmm19900403@126.com.
[Ti] Título:Lactulose production from efficient isomerization of lactose catalyzed by recyclable sodium aluminate.
[So] Source:Food Chem;233:151-158, 2017 Oct 15.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An efficient strategy for the synthesis of high-purity lactulose through chemical isomerization of lactose was developed using recyclable catalyst sodium aluminate. Maximum yield of 85.45±1.79% was obtained from 35% (w/v) of lactose using a 1:1M ratio of NaAlO -lactose after reaction at 60°C and pH 12 for 50min, with a purity ratio (Pu) of approximately 95%. Al(OH) precipitation from lactulose syrup through pH adjustment showing a superior decolorizing efficiency was implemented, which simplified the removal of catalyst and provided a convenient approach to achieve catalyst recovery. After dilution by 5 folds, nearly 98.5% of catalyst was removed through centrifugation and 85.50±1.81% of lactulose was recovered. Modified recycle use of catalyst without lactulose loss was carried out, after five consecutive recycles, total yield of lactulose (TY ) and new yield of lactulose (NY ) were of 80.44±1.05% and 73.87±0.50%, respectively, reflecting a high stability by using this recyclable methodology.
[Mh] Termos MeSH primário: Lactulose/química
[Mh] Termos MeSH secundário: Compostos de Alumínio
Catálise
Isomerismo
Lactose
Compostos de Sódio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aluminum Compounds); 0 (Sodium Compounds); 0 (sodium aluminate); 4618-18-2 (Lactulose); J2B2A4N98G (Lactose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE


  10 / 2309 MEDLINE  
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[PMID]:28529145
[Au] Autor:Guerra-Moreno A; Hanna J
[Ad] Endereço:Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States.
[Ti] Título:Induction of proteotoxic stress by the mycotoxin patulin.
[So] Source:Toxicol Lett;276:85-91, 2017 Jul 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Patulin is a naturally occurring mycotoxin produced by a number of molds and may contaminate a wide variety of food products. In practice, patulin's main societal relevance concerns apple juice and its products. Multiple advisory bodies, including the U.S. Food and Drug Administration and the World Health Organization, recommend that producers monitor and limit patulin levels in apple juice products. The mechanism of patulin toxicity remains largely unknown. Here we show that patulin induces proteotoxic stress in the yeast S. cerevisiae. The transcription factor Rpn4 controls the abundance of the proteasome, the complex multisubunit protease that destroys proteins, including misfolded proteins. Rpn4 protein is strongly induced by patulin, and Rpn4 levels normalize over time, consistent with homeostatic regulation. A rpn4Δ mutant is highly sensitive to patulin, confirming the physiologic relevance of this response. Rpn4 is known to be regulated both transcriptionally and post-translationally. Patulin induces both pathways of regulation, but the post-transcriptional pathway predominates in controlling Rpn4 protein levels. These results indicate that proteotoxicity represents a major aspect of patulin toxicity. They not only have implications for patulin detoxification but in addition suggest the possibility of some potentially useful patulin applications.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/metabolismo
Microbiologia de Alimentos
Patulina/toxicidade
Complexo de Endopeptidases do Proteassoma/efeitos dos fármacos
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/efeitos dos fármacos
Estresse Fisiológico/efeitos dos fármacos
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Arsenitos/toxicidade
Proteínas de Ligação a DNA/genética
Regulação Fúngica da Expressão Gênica
Mutação
Complexo de Endopeptidases do Proteassoma/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
Proteínas de Saccharomyces cerevisiae/genética
Compostos de Sódio/toxicidade
Fatores de Tempo
Fatores de Transcrição/genética
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenites); 0 (DNA-Binding Proteins); 0 (RPN4 protein, S cerevisiae); 0 (Saccharomyces cerevisiae Proteins); 0 (Sodium Compounds); 0 (Transcription Factors); 48OVY2OC72 (sodium arsenite); 95X2BV4W8R (Patulin); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE



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