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Pesquisa : D12.776.543.585.475 [Categoria DeCS]
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[PMID]:29413990
[Au] Autor:Kelly J; Murphy JE
[Ad] Endereço:Mitochondrial Biology & Radiation Research Centre, Dept. of Life Sciences, Institute of Technology Sligo, Ash Lane, Sligo, Ireland. Electronic address: janiskelly@mail.itsligo.ie.
[Ti] Título:Mitochondrial gene expression changes in cultured human skin cells following simulated sunlight irradiation.
[So] Source:J Photochem Photobiol B;179:167-174, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure of skin to simulated sunlight irradiation (SSI) has being extensively researched and shown to be the main cause for changes in the skin including changes in cellular function and generation of reactive oxygen species (ROS). This oxidative stress can subsequently exert downstream effects and the subcellular compartments most affected by this oxidative stress are mitochondria. The importance of functional mitochondrial morphology is apparent as morphological defects are related to many human diseases including diabetes mellitus, liver disease, neurodegenerative diseases, aging and cancer. OBJECTIVE: The main objective of this study was to evaluate solar radiation-induced changes in mitochondrial gene expression in human skin cells using a Q-Sun solar simulator to deliver a close match to the intensity of summer sunlight. METHODS: Spontaneously immortalised human skin epidermal keratinocytes (HaCaT) and Human Dermal Fibroblasts (HDFn) were divided into two groups. Group A were irradiated once and Group B twice 7days apart; following irradiation, mitochondrial gene expression was evaluated 1, 4 and 7days post primary exposure for group A and 1, 4, 7 and 14days post-secondary exposure for group B. RESULTS: Both the epidermal and dermal cells displayed significant reduced expression of the genes analysed for mitochondrial morphology and function; however, epidermal cells displayed this reduction post SSI earlier then dermal cells at multiple time points. CONCLUSION: The data presented here reinforces the fact that epidermal cells, while displaying a heightened sensitivity to sunlight, are less prone to changes in gene expression, while dermal cells, which appear to be more resilient are possibly more prone to genomic instability and mitochondrial damage.
[Mh] Termos MeSH primário: Expressão Gênica/efeitos da radiação
Mitocôndrias/genética
Luz Solar
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/genética
ATPases Associadas a Diversas Atividades Celulares/metabolismo
Linhagem Celular
Derme/citologia
Epiderme/citologia
GTP Fosfo-Hidrolases/genética
GTP Fosfo-Hidrolases/metabolismo
Seres Humanos
Queratinócitos/citologia
Queratinócitos/metabolismo
Queratinócitos/efeitos da radiação
Metaloendopeptidases/genética
Metaloendopeptidases/metabolismo
Mitocôndrias/efeitos da radiação
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (superoxide dismutase 2); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (YME1L1 protein, human); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (MFN2 protein, human); EC 3.6.1.- (OPA1 protein, human); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities); EC 3.6.5.- (Mfn1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


  2 / 3130 MEDLINE  
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[PMID]:29288949
[Au] Autor:Elkamhawy A; Park JE; Hassan AHE; Pae AN; Lee J; Park BG; Roh EJ
[Ad] Endereço:Chemical Kinomics Research Center, Korea Institute of Science and Technology (KIST), Seoul 02792, Republic of Korea; Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt.
[Ti] Título:Synthesis and evaluation of 2-(3-arylureido)pyridines and 2-(3-arylureido)pyrazines as potential modulators of Aß-induced mitochondrial dysfunction in Alzheimer's disease.
[So] Source:Eur J Med Chem;144:529-543, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A series of 2-(3-arylureido)pyridines and 2-(3-benzylureido)pyridines were synthesized and evaluated as potential modulators for amyloid beta (Aß)-induced mitochondrial dysfunction in Alzheimer's disease (AD). The blocking activities of forty one small molecules against Aß-induced mitochondrial permeability transition pore (mPTP) opening were evaluated by JC-1 assay which measures the change of mitochondrial membrane potential (ΔΨm). The inhibitory activity of twenty five compounds against Aß-induced mPTP opening was superior to that of the standard cyclosporin A (CsA). Six hit compounds have been identified as likely safe in regards to mitochondrial and cellular safety and subjected to assessment for their protective effect against Aß-induced deterioration of ATP production and cytotoxicity. Among them, compound 7fb has been identified as a lead compound protecting neuronal cells against 67% of neurocytotoxicity and 43% of suppression of mitochondrial ATP production induced by 5 µM concentrations of Aß. Using CDocker algorithm, a molecular docking model presented a plausible binding mode for these compounds with cyclophilin D (CypD) receptor as a major component of mPTP. Hence, this report presents compound 7fb as a new nonpeptidyl mPTP blocker which would be promising for further development of Alzheimer's disease (AD) therapeutics.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/antagonistas & inibidores
Mitocôndrias/efeitos dos fármacos
Pirazinas/farmacologia
Piridinas/farmacologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/metabolismo
Morte Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Mitocôndrias/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Simulação de Acoplamento Molecular
Estrutura Molecular
Pirazinas/síntese química
Pirazinas/química
Piridinas/síntese química
Piridinas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Mitochondrial Membrane Transport Proteins); 0 (Pyrazines); 0 (Pyridines); 0 (mitochondrial permeability transition pore)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  3 / 3130 MEDLINE  
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[PMID]:29357290
[Au] Autor:Fujimoto N; Kitamura S; Uramaru N; Miyagawa S; Iguchi T
[Ad] Endereço:Institute for Radiation Biology and Medicine (RIRBM), Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. Electronic address: nfjm@hiroshima-u.ac.jp.
[Ti] Título:Identification of hepatic thyroid hormone-responsive genes in neonatal rats: Potential targets for thyroid hormone-disrupting chemicals.
[So] Source:Toxicol Lett;286:48-53, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:There have been many concerns about the possible adverse effects of thyroid hormone-disrupting chemicals in the environment. Because thyroid hormones are essential for regulating the growth and differentiation of many tissues, disruption of thyroid hormones during the neonatal period of an organism might lead to permanent effects on that organism. We postulated that there are target genes that are sensitive to thyroid hormones particularly during the neonatal period and that would thus be susceptible to thyroid hormone-disrupting chemicals. Global gene expression analysis was used to identify these genes in the liver of rat neonates. The changes in hepatic gene expression were examined 24 h after administering 1.0, 10, and 100 ng/g body weight (bw) triiodothyronine (T3) to male rats on postnatal day 3. Thirteen upregulated and four downregulated genes were identified in the neonatal liver. Among these, Pdp2 and Slc25a25 were found to be upregulated and more sensitive to T3 than the others, whereas Cyp7b1 and Hdc were found to be downregulated even at the lowest dose of 1.0 ng/g bw T3. Interestingly, when the responses of gene expression to T3 were examined in adult rats (8-week old), one-third of them did not respond to T3. The environmental chemicals with thyroid hormone-like activity, hydroxylated polybrominated diphenyl ethers, were then administered to neonatal rats to examine the effects on expression of the identified genes. The results showed that these chemicals were indeed capable of changing the expression of Slc25a25 and Hdc. Our results demonstrated a series of hepatic T3-responsive genes that are more sensitive to hormones during the neonatal period than during adulthood. These genes might be the potential targets of thyroid hormone-disrupting chemicals in newborns.
[Mh] Termos MeSH primário: Disruptores Endócrinos/toxicidade
Regulação da Expressão Gênica/efeitos dos fármacos
Fígado/efeitos dos fármacos
Tri-Iodotironina/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Família 7 do Citocromo P450/genética
Família 7 do Citocromo P450/metabolismo
Relação Dose-Resposta a Droga
Perfilação da Expressão Gênica/métodos
Histidina Descarboxilase/genética
Histidina Descarboxilase/metabolismo
Fígado/metabolismo
Masculino
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Piruvato Desidrogenase (Lipoamida)-Fosfatase/genética
Piruvato Desidrogenase (Lipoamida)-Fosfatase/metabolismo
Ratos Endogâmicos F344
Medição de Risco
Esteroide Hidroxilases/genética
Esteroide Hidroxilases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocrine Disruptors); 0 (Mitochondrial Membrane Transport Proteins); 0 (Slc25a25 protein, rat); 06LU7C9H1V (Triiodothyronine); EC 1.14.- (Steroid Hydroxylases); EC 1.14.13.100 (Cyp7b1 protein, rat); EC 1.14.14.23 (Cytochrome P450 Family 7); EC 3.1.3.43 (Pyruvate Dehydrogenase (Lipoamide)-Phosphatase); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


  4 / 3130 MEDLINE  
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[PMID]:29222049
[Au] Autor:Park J; Han JH; Myung SH; Seo YW; Kim TH
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Chosun University School of Medicine, 309 Pilmoon-Daero, Dong-Gu, Gwang-Ju, 61452 Republic of Korea.
[Ti] Título:MTD-like motif of a BH3-only protein, BNIP1, induces necrosis accompanied by an intracellular calcium spike.
[So] Source:Biochem Biophys Res Commun;495(2):1661-1667, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mitochondrial targeting domain (MTD) of Noxa has necrosis-inducing activity when conjugated with cell-penetrating peptide (CPP). In this study, we report another MTD-like motif, B1MLM, found in BNIP1, a pro-apoptotic BH3-only protein found in the endoplasmic reticulum membrane. The B1MLM peptide, conjugated with CPP, induced necrosis in a way similar to that of R8:MTD. R8:B1MLM caused an intracellular calcium spike, mitochondrial reactive oxygen species generation, and mitochondrial fragmentation. The cytosolic calcium spike was likely due to the opening of the mitochondrial permeability transition pore.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Proteínas Proto-Oncogênicas c-bcl-2/química
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sequência de Aminoácidos
Peptídeos Penetradores de Células/química
Peptídeos Penetradores de Células/metabolismo
Células HeLa
Seres Humanos
Mitocôndrias/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Necrose
Proteínas Proto-Oncogênicas c-bcl-2/genética
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BNIP1 protein, human); 0 (Cell-Penetrating Peptides); 0 (Mitochondrial Membrane Transport Proteins); 0 (PMAIP1 protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Reactive Oxygen Species); 0 (mitochondrial permeability transition pore)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


  5 / 3130 MEDLINE  
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[PMID]:29223393
[Au] Autor:Korotkov SM; Konovalova SA; Nesterov VP; Brailovskaya IV
[Ad] Endereço:Sechenov Institute of Evolutionary Physiology and Biochemistry, The Russian Academy of Sciences, Thorez pr. 44, 194223 St. Petersburg, Russia. Electronic address: korotkov@SK1645.spb.edu.
[Ti] Título:Mersalyl prevents the Tl -induced permeability transition pore opening in the inner membrane of Ca -loaded rat liver mitochondria.
[So] Source:Biochem Biophys Res Commun;495(2):1716-1721, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It was earlier shown that the calcium load of rat liver mitochondria in medium containing TlNO and KNO resulted in the Tl -induced mitochondrial permeability transition pore (MPTP) opening in the inner membrane. This opening was accompanied by an increase in swelling and membrane potential dissipation and a decrease in state 3, state 4, and 2,4-dinitrophenol-uncoupled respiration. This respiratory decrease was markedly leveled by mersalyl (MSL), the phosphate symporter (PiC) inhibitor which poorly stimulated the calcium-induced swelling, but further increased the potential dissipation. All of these effects of Ca and MSL were visibly reduced in the presence of the MPTP inhibitors (ADP, N-ethylmaleimide, and cyclosporine A). High MSL concentrations attenuated the ability of ADP to inhibit the MPTP. Our data suggest that the PiC can participate in the Tl -induced MPTP opening in the inner membrane of Ca -loaded rat liver mitochondria.
[Mh] Termos MeSH primário: Mersalil/farmacologia
Mitocôndrias Hepáticas/efeitos dos fármacos
Mitocôndrias Hepáticas/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Tálio/farmacologia
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Técnicas In Vitro
Transporte de Íons/efeitos dos fármacos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Membranas Mitocondriais/efeitos dos fármacos
Membranas Mitocondriais/metabolismo
Dilatação Mitocondrial/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (mitochondrial permeability transition pore); 5X1IO031V8 (Mersalyl); AD84R52XLF (Thallium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


  6 / 3130 MEDLINE  
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[PMID]:29235789
[Au] Autor:Danylovych YV; Chunikhin AY; Danylovych GV; Kolomiets OV
[Ti] Título:The use of the Petri net method in the simulation modeling of mitochondrial swelling.
[So] Source:Ukr Biochem J;88(4):66-74, 2016 Jul-Aug.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Using photon correlation spectroscopy, which allows investigating changes in the hydrodynamic dia­meter of the particles in suspension, it was shown that ultrahigh concentrations of Ca2+ (over 10 mM) induce swelling of isolated mitochondria. An increase in hydrodynamic diameter was caused by an increase of non-specific mitochondrial membrane permeability to Ca ions, matrix Ca2+ overload, activation of ATP- and Ca2+-sensitive K+-channels, as well as activation of cyclosporin-sensitive permeability transition pore. To formalize the experimental data and to assess conformity of experimental results with theoretical predictions we developed a simulation model using the hybrid functional Petri net method.
[Mh] Termos MeSH primário: Cálcio/farmacologia
Ciclosporina/farmacologia
Mitocôndrias/efeitos dos fármacos
Dilatação Mitocondrial/efeitos dos fármacos
Modelos Biológicos
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Cátions Bivalentes
Permeabilidade da Membrana Celular/efeitos dos fármacos
Simulação por Computador
Feminino
Transporte de Íons
Canais KATP/metabolismo
Cinética
Mitocôndrias/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Miométrio/química
Miométrio/metabolismo
Canais de Potássio Cálcio-Ativados/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Divalent); 0 (KATP Channels); 0 (Mitochondrial Membrane Transport Proteins); 0 (Potassium Channels, Calcium-Activated); 0 (mitochondrial permeability transition pore); 83HN0GTJ6D (Cyclosporine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.04.066


  7 / 3130 MEDLINE  
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[PMID]:28743501
[Au] Autor:Cui C; Lin H; Shi Y; Pan R
[Ad] Endereço:Department of Aesthetic Plastic Surgery and Laser Medicine, Beijing Anzhen Hospital, Capital Medical University, Anzhen Road #2, Chaoyang District, Beijing 100029, China. Electronic address: 15501008735@163.com.
[Ti] Título:Hypoxic postconditioning attenuates apoptosis via inactivation of adenosine A receptor through NDRG3-Raf-ERK pathway.
[So] Source:Biochem Biophys Res Commun;491(2):277-284, 2017 09 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In recent years, many studies have demonstrated that endogenous adenosine induced by ischemia postconditioning reduces apoptosis in animal and cell models, but no study has clearly elucidated the effects of hypoxia postconditioning (HPC) in human dermal microvascular endothelial cells (HDMECs) of flaps, and the subtype of adenosine receptors involved remains unknown. In our study, we sought to identify the roles of adenosine A receptor, NDRG3 (N-myc downstream-regulated gene 3) and Raf-ERK pathway in the anti-apoptotic effects of hypoxia postconditioning. METHODS: Human dermal microvascular endothelial cells were put into a hypoxic incubator (94% N + 5% CO + 1% O ) for 8 h (hypoxia), and followed 24 h of normoxic culture with 95% air and 5% CO (reoxygenation). Hypoxia postconditioning model of HDMECs was achieved as follows: Before HDMECs were put into a normoxic incubator, HDMECs were treated by three cycles of 5 min of brief reoxygenation and 5 min of re-hypoxia. Opening level of mitochondrial permeability transition pore and change of mitochondrial membrane potential were detected with related Kit. The protein expressions of mitochondrion apoptosis, adenosine A receptor and NDRG3-Raf-ERK pathway were measured by western blot. RESULT: Hypoxia/reoxygenation (H/R) resulted in injury in HDMRCs as evidenced by an increase in apoptosis percentage, mitochondrial membrane permeability and an increase in expression of pro-apoptosis proteins (Bax, c-caspase-3 and cytochrom C), meanwhile, hypoxia/reoxygenation increased expression of A receptor, NDRG3, p-c-Raf, p-ERK, which was significantly attenuated by hypoxia postconditioning treatment. Moreover, Hypoxia/reoxygenation (H/R) resulted in a decrease in expression of anti-apoptotic protein (Bcl-2). However, the protective effect of hypoxia postconditioning treatment could be inhibited by adding CGS21680, a selective adenosine A receptor agonist (all P values < 0.05).
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Células Endoteliais/efeitos dos fármacos
Pós-Condicionamento Isquêmico
Proteínas do Tecido Nervoso/genética
Oxigênio/farmacologia
Receptor A2A de Adenosina/genética
Quinases raf/genética
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/farmacologia
Agonistas do Receptor A2 de Adenosina/farmacologia
Apoptose/genética
Caspase 3/genética
Caspase 3/metabolismo
Hipóxia Celular
Derme/irrigação sanguínea
Derme/citologia
Derme/efeitos dos fármacos
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Potencial da Membrana Mitocondrial
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Modelos Biológicos
Proteínas do Tecido Nervoso/metabolismo
Fenetilaminas/farmacologia
Cultura Primária de Células
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Receptor A2A de Adenosina/metabolismo
Retalhos Cirúrgicos/irrigação sanguínea
Proteína X Associada a bcl-2/genética
Proteína X Associada a bcl-2/metabolismo
Quinases raf/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adenosine A2 Receptor Agonists); 0 (BAX protein, human); 0 (BCL2 protein, human); 0 (Mitochondrial Membrane Transport Proteins); 0 (NDRG3 protein, human); 0 (Nerve Tissue Proteins); 0 (Phenethylamines); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptor, Adenosine A2A); 0 (bcl-2-Associated X Protein); 0 (mitochondrial permeability transition pore); 120225-54-9 (2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine); EC 2.7.11.1 (raf Kinases); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); K72T3FS567 (Adenosine); S88TT14065 (Oxygen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


  8 / 3130 MEDLINE  
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[PMID]:28409819
[Au] Autor:Ghosh P; Bhoumik A; Saha S; Mukherjee S; Azmi S; Ghosh JK; Dungdung SR
[Ad] Endereço:Sperm Biology Laboratory, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, West Bengal, India.
[Ti] Título:Spermicidal efficacy of VRP, a synthetic cationic antimicrobial peptide, inducing apoptosis and membrane disruption.
[So] Source:J Cell Physiol;233(2):1041-1050, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Presently available contraceptives are mostly hormonal or detergent in nature with numerous side effects like irritation, lesion, inflammation in vagina, alteration of body homeostasis, etc. Antimicrobial peptides with spermicidal activity but without adverse effects may be suitable alternatives. In the present study, spermicidal activity of a cationic antimicrobial peptide VRP on human spermatozoa has been elucidated. Progressive forward motility of human spermatozoa was instantly stopped after 100 µM VRP treatment and at 350 µM, all kinds of sperm motility ceased within 20 s as assessed by the Sander-Cramer assay. The spermicidal effect was confirmed by eosin-nigrosin assay and HOS test. VRP treatment (100 µM) in human spermatozoa induced both the intrinsic and extrinsic pathways of apoptosis. TUNEL assay showed VRP treatment significantly disrupted the DNA integrity and changed the mitochondrial membrane permeability as evident from MPTP assay. AFM and SEM results depicted ultra structural changes including disruption of the acrosomal cap and plasma membrane of the head and midpiece region after treatment with 350 µM VRP. MTT assay showed after treatments with 100 and 350 µM of VRP for 24 hr, a substantial amount of Lactobacillus acidophilus (about 90% and 75%, respectively) remained viable. Hence, VRP being a small synthetic peptide with antimicrobial and spermicidal activity but tolerable to normal vaginal microflora, may be a suitable target for elucidating its contraceptive potentiality.
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/farmacologia
Apoptose/efeitos dos fármacos
Membrana Celular/efeitos dos fármacos
Peptídeos/farmacologia
Espermicidas/farmacologia
Espermatozoides/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acrossomo/efeitos dos fármacos
Acrossomo/metabolismo
Acrossomo/ultraestrutura
Membrana Celular/metabolismo
Membrana Celular/ultraestrutura
Relação Dose-Resposta a Droga
Seres Humanos
Lactobacillus/efeitos dos fármacos
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Viabilidade Microbiana/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Membranas Mitocondriais/efeitos dos fármacos
Membranas Mitocondriais/metabolismo
Membranas Mitocondriais/ultraestrutura
Permeabilidade
Peça Intermédia do Espermatozoide/efeitos dos fármacos
Peça Intermédia do Espermatozoide/metabolismo
Peça Intermédia do Espermatozoide/ultraestrutura
Motilidade Espermática/efeitos dos fármacos
Espermatozoides/metabolismo
Espermatozoides/ultraestrutura
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (Mitochondrial Membrane Transport Proteins); 0 (Peptides); 0 (Spermatocidal Agents); 0 (mitochondrial permeability transition pore); 25609-85-2 (polyvaline)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25958


  9 / 3130 MEDLINE  
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[PMID]:28942440
[Au] Autor:Zhou X; Liang L; Zhao Y; Zhang H
[Ad] Endereço:Department of Cardiology, The First People's Hospital of Yunnan, Kunming, China.
[Ti] Título:Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling.
[So] Source:J Vasc Res;54(5):299-308, 2017.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: This study aimed to investigate whether epigallocatechin-3-gallate (EGCG) shows antioxidant activity against angiotensin II (Ang II)-induced human umbilical vein endothelial cell (HUVEC) apoptosis. MATERIALS AND METHODS: The viability of HUVECs was revealed by MTT and LDH assay. The cell apoptosis was detected by FITC-PI assay. A fluorescent probe assay was used to measure the reactive oxygen species (ROS) generation in HUVECs. Mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential, and caspase-3, -4, -8, -9 activities were also measured. RESULTS: We found that Ang II treatment increased the generation of ROS, enhanced MPTP opening and cytochrome c release, activated caspase-3/9, and consequently induced HUVEC apoptosis. EGCG treatment-suppressed Ang II induces the oxidative stress of HUVECs and mitochondria-related cell apoptosis. We also showed that the antioxidant activity pathway, including cytochrome c release, MPTP opening, and caspase-3/9 activation, is a key endogenous defensive system in HUVECs, provoking Ang II exposure. Our study revealed that increased expression of Nrf2 by EGCG could partially repress Ang II-induced injury effects. CONCLUSIONS: All of our findings indicated that EGCG treatment provides a protective effect for Ang II-induced HUVEC apoptosis by decreasing oxidative stress and ameliorating mitochondrial injury.
[Mh] Termos MeSH primário: Angiotensina II/toxicidade
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Catequina/análogos & derivados
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Caspase 9/metabolismo
Catequina/farmacologia
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citocromos c/metabolismo
Citoproteção
Relação Dose-Resposta a Droga
Células Endoteliais da Veia Umbilical Humana/enzimologia
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/enzimologia
Mitocôndrias/patologia
Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Mitochondrial Membrane Transport Proteins); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (Reactive Oxygen Species); 0 (mitochondrial permeability transition pore); 11128-99-7 (Angiotensin II); 8R1V1STN48 (Catechin); 9007-43-6 (Cytochromes c); BQM438CTEL (epigallocatechin gallate); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP9 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE
[do] DOI:10.1159/000479873


  10 / 3130 MEDLINE  
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[PMID]:28827831
[Au] Autor:Wenger C; Oeljeklaus S; Warscheid B; Schneider A; Harsman A
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Bern, Freiestrasse 3, Bern, Switzerland.
[Ti] Título:A trypanosomal orthologue of an intermembrane space chaperone has a non-canonical function in biogenesis of the single mitochondrial inner membrane protein translocase.
[So] Source:PLoS Pathog;13(8):e1006550, 2017 Aug.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial protein import is essential for Trypanosoma brucei across its life cycle and mediated by membrane-embedded heterooligomeric protein complexes, which mainly consist of trypanosomatid-specific subunits. However, trypanosomes contain orthologues of small Tim chaperones that escort hydrophobic proteins across the intermembrane space. Here we have experimentally analyzed three novel trypanosomal small Tim proteins, one of which contains only an incomplete Cx3C motif. RNAi-mediated ablation of TbERV1 shows that their import, as in other organisms, depends on the MIA pathway. Submitochondrial fractionation combined with immunoprecipitation and BN-PAGE reveals two pools of small Tim proteins: a soluble fraction forming 70 kDa complexes, consistent with hexamers and a second fraction that is tightly associated with the single trypanosomal TIM complex. RNAi-mediated ablation of the three proteins leads to a growth arrest and inhibits the formation of the TIM complex. In line with these findings, the changes in the mitochondrial proteome induced by ablation of one small Tim phenocopy the effects observed after ablation of TbTim17. Thus, the trypanosomal small Tims play an unexpected and essential role in the biogenesis of the single TIM complex, which for one of them is not linked to import of TbTim17.
[Mh] Termos MeSH primário: Proteínas de Membrana Transportadoras/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Chaperonas Moleculares/metabolismo
Transporte Proteico/fisiologia
Trypanosoma brucei brucei/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Northern Blotting
Cromatografia Líquida de Alta Pressão
Imunoprecipitação
Estágios do Ciclo de Vida
Espectrometria de Massas
Microscopia de Fluorescência
Membranas Mitocondriais/metabolismo
Trypanosoma brucei brucei/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Transport Proteins); 0 (Mitochondrial Membrane Transport Proteins); 0 (Molecular Chaperones)
[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:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006550



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