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Pesquisa : A11.284.430.214.190.875.564 [Categoria DeCS]
Referências encontradas : 280 [refinar]
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Id: biblio-907783
Autor: Ospina-Medina, Luisa F; Cardona-Maya, Walter D.
Título: Evaluación del potencial de membrana mitocondrial en espermatozoides humanos capacitados / Mitochondrial membrane potential evaluation in capacitated human sperm
Fonte: Med. lab;21(7-8):375-382, 2015. tab, graf.
Idioma: es.
Resumo: Introducción: los espermatozoides humanos durante su viaje por el tracto reproductivo sufren el procesode capacitación espermática, evento indispensable para la fecundación y que se ha relacionado con cambios en el potencial de membrana mitocondrial. Objetivos: evaluar el efecto de la capacitaciónespermática sobre el potencial de membrana mitocondrial en espermatozoides humanos. Materiales y métodos: se realizó un estudio in vitro en el cual se seleccionaron los espermatozoides puros de nueve voluntarios, los cuales se sometieron a condiciones capacitantes durante seis horas. Posteriormente, se evaluó el efecto de la capacitación sobre el estado del potencial de membrana mitocondrial usando el colorante DiOC6(3) por citometría de flujo. Resultados: de las nueve muestras seminales evaluadas cinco presentaron mayor intensidad media de fluorescencia en el potencial de membrana mitocondrial poscapacitación. Todas las muestras seminales mostraron parámetros normales y no presentaron cambios en la movilidad y la viabilidad espermática durante la selección y la capacitación espermática in vitro. Conclusiones: las modificaciones en el potencial de membrana mitocondrial en respuesta al proceso de capacitación demuestra que existen diferentes poblaciones espermáticas en el eyaculado humano; entender cuál está relacionada con el proceso reproductivo exitoso permitirá aumentar la probabilidad de embarazos.

Introduction: human spermatozoa during their journey through the reproductive tract undergo the capacitation process, an essential event for the fertilization and which has been related with changesin membrane mitochondrial potential. Objective: To evaluate the effect of capacitation process on mitochondrial membrane potential in human sperm. Materials and methods: An in vitro study in which pure sperm from nine semen samples were incubated in capacitated conditions for six hours. Subsequently, the capacitation effect on the state of mitochondrial membrane potential using DiOC6(3) dye through flow cytometry were evaluated. Results: Nine semen samples were evaluated; five had higher mean fluorescence intensity in the mitochondrial membrane potential post capacitation.All semen samples had normal seminal parameters and none of them showed changes in motility and sperm viability during recovery and in vitro capacitation. Conclusions: Changes in the mitochondrial membrane potential in response to the capacitation process shows that there are different sperm populations in the human ejaculated; understand which are related to the successful reproductive process will increase the likelihood of pregnancy.
Descritores: Fertilidade
Mitocôndrias
Capacitação Espermática
Espermatozoides
Limites: Humanos
Tipo de Publ: Estudo de Avaliação
Responsável: CO373.9 - EDIMECO - Editora Médica Colombiana S.A.


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Id: biblio-1146375
Autor: FROIDEVAUX, Jérémy SP; ROEMER, Charlotte; MARCHAND, Clément LE; MARTÍ-CARRERAS, Joan; MAES, Piet; RUFRAY, Vincent; URIOT, Quentin; URIOT, Sylvain; LÓPEZ-BAUCELLS, Adrià.
Título: Second capture of Promops centralis (Chiroptera) in French Guiana after 28 years of mist-netting and description of its echolocation and distress calls
Fonte: Acta amaz;50(4):327-334, out. - dez. 2020.
Idioma: en.
Resumo: la literatura científica no encontramos información muy detallada sobre especies de murciélago esquivas como las de la família Molossidae. Esta carencia condiciona y obstaculiza los esfuerzos de conservación tanto a escala local como global. El desarrollo reciente de nuevas tecnologías diseñadas específicamente para muestrear quirópteros, como los detectores de ultrasonidos pasivos o los reclamos acústicos mediante el uso de llamadas de alta frecuencia, ha incrementado nuestro conocimiento sobre su ecología y distribución. Además, ha permitido a los investigadores obtener nuevos datos que eran prácticamente imposibles de conseguir en el pasado. Llevamos a cabo una evaluación rápida de diversidad quiropterológica en la Guayana Francesa, utilizando reclamos cústicos con el objetivo de capturar especies insectívoras de vuelo alto. En este estudio, aportamos la segunda y tercera captura de Promops centralis (Chiroptera, Molossidae) para Guayana Francesa después de 28 años desde sus primeras y únicas capturas hasta ahora. Uno de los indivíduos capturados fue una hembra poslactante, el primer registro de reproducción de la especie. Aportamos (i) datos morfométricos, bioacústicos (incluyendo las llamadas de alarma típicas de la especie) y fotografías de detalles para facilitarsu identificación; y (ii) las secuencias de COI y CytB de los dos individuos (las primeras secuencias mitocondriales para la Guayana Francesa). (AU)
Descritores: Quirópteros
Ecossistema Amazônico
Mitocôndrias
Responsável: BR6.1 - BCS - Biblioteca de Ciências da Saúde


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Id: biblio-1142417
Autor: Peng, Yan; Yang, Xinming; Luo, Xi; Liu, Chunhong; Cao, Xia; Wang, Hongyan; Guo, Liyuan.
Título: Novel mechanisms underlying anti-polycystic ovary like syndrome effects of electroacupuncture in rats: suppressing SREBP1 to mitigate insulin resistance, mitochondrial dysfunction and oxidative stress
Fonte: Biol. Res;53:50, 2020. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Postdoctoral Science Foundation of China; . Heilongjiang University of Chinese Medicine; . Heilongjiang Provincial Government.
Resumo: BACKGROUND: Acupuncture, a therapy of traditional Chinese medicine, is confirmed to exert the therapeutic action on polycystic ovary syndrome (PCOS). However, the detailed therapeutic mechanisms of acupuncture in PCOS remain ambiguous. In this study, we further investigated whether electroacupuncture (EA) alleviated PCOS-like symptoms in rats via regulating a metabolic regulator, sterol regulatory element binding protein-1 (SREBP1). Methods: The PCOS-like rat model was built by hypodermic injection with dehydroepiandrosterone (DHEA). The rats were subjected to EA intervention (ST29 and SP6 acupuncture points) for 5 weeks. Primary granulosa cells were isolated from control and PCOS-like rats for evaluating insulin resistance, mitochondrial dysfunction and oxidative stress in vitro. RESULTS: The expression of SREBP1 was increased in PCOS-like rats, which was suppressed by EA treatment. In addition, lentivirus-mediated overexpression of SREBP1 restrained EA treatment-induced improvement in pathological changes, serum hormone levels and insulin resistance in rats. In addition, overexpression of SREBP1 repressed insulin-stimulated phosphorylation of insulin receptor ß (IR) and AKT in primary granulosa cells. Moreover, upregulation of SREBP1 further exacerbated mitochondrial dysfunction and oxidative stress in granulosa cells isolated from PCOS-like rats. Mechanically, EA treatment suppressed SREBP1 expression through inducing the activation of AMP-activated protein kinase (AMPK) signaling pathway in PCOS-like rats. CONCLUSION: EA intervention alleviated PCOS-like symptoms in rats via improving IR, mitochondrial dysfunction and oxidative stress through regulating SREBP1, a lipid metabolism regulator. Our findings illuminate the novel protective mechanisms of EA in the treatment of PCOS.
Descritores: Síndrome do Ovário Policístico/induzido quimicamente
Síndrome do Ovário Policístico/terapia
Resistência à Insulina
Eletroacupuntura
Estresse Oxidativo
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Mitocôndrias/patologia
-Ratos Sprague-Dawley
Desidroepiandrosterona
Limites: Animais
Feminino
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1053221
Autor: Wang, Lamei; Ma, Sen; Ding, Qiang; Wang, Xiaolong; Chen, Yulin.
Título: CRISPR/Cas9-mediated MSTN gene editing induced mitochondrial alterations in C2C12 myoblast cells
Fonte: Electron. j. biotechnol;40:30-39, July. 2019. ilus, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . National Key Research and Development Program; . Key Research Program of Shaanxi Province.
Resumo: Background: Myostatin (MSTN) negatively regulates muscle mass and is a potent regulator of energy metabolism. However, MSTN knockout have affect mitochondrial function. This research assessed the mitochondrial energy metabolism of Mstn−/+ KO cells, and wondered whether the mitochondria biogenesis are affected. Results: In this study, we successfully achieved Mstn knockout in skeletal muscle C2C12 cells using a CRISPR/Cas9 system and measured proliferation and differentiation using the Cell-Counting Kit-8 assay and qPCR, respectively. We found that MSTN dysfunction could promote proliferation and differentiation compared with the behaviour of wild-type cells. Moreover, Mstn KO induced an increase in KIF5B expression. The mitochondrial content was significantly increased in Mstn KO C2C12 cells, apparently associated with the increases in PGC-1α, Cox1, Cox2, ND1 and ND2 expression. However, no differences were observed in glucose consumption and lactate production. Interestingly, Mstn KO C2C12 cells showed an increase in IL6 and a decrease in TNF-1α levels. Conclusion: These findings indicate that MSTN regulates mitochondrial biogenesis and metabolism. This gene-editing cells provided favourable evidence for animal breeding and metabolic diseases.
Descritores: Miostatina/genética
Mitocôndrias/genética
Mitocôndrias/metabolismo
-Biogênese de Organelas
Immunoblotting
Diferenciação Celular
Músculo Esquelético/citologia
Músculo Esquelético/metabolismo
Mioblastos/citologia
Mioblastos/metabolismo
MicroRNAs
Proliferação de Células
Sistemas CRISPR-Cas
Citometria de Fluxo
Edição de Genes
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-839198
Autor: Kohatsu, Andréa A N; Silva, Flávia A J; Francisco, Acácio I; Rimoldi, Aline; Silva, Marco T A; Vargas, Maria D; Rosa, João A da; Cicarelli, Regina M B.
Título: Differential expression on mitochondrial tryparedoxin peroxidase (mTcTXNPx) in Trypanosoma cruzi after ferrocenyl diamine hydrochlorides treatments
Fonte: Braz. j. infect. dis;21(2):125-132, Mar.-Apr. 2017. tab, graf.
Idioma: en.
Projeto: FAPESP.
Resumo: Abstract Resistance to benznidazole in certain strains of Trypanosoma cruzi may be caused by the increased production of enzymes that act on the oxidative metabolism, such as mitochondrial tryparedoxin peroxidase which catalyses the reduction of peroxides. This work presents cytotoxicity assays performed with ferrocenyl diamine hydrochlorides in six different strains of T. cruzi epimastigote forms (Y, Bolivia, SI1, SI8, QMII, and SIGR3). The last four strains have been recently isolated from triatominae and mammalian host (domestic cat). The expression of mitochondrial tryparedoxin peroxidase was analyzed by the Western blotting technique using polyclonal antibody anti mitochondrial tryparedoxin peroxidase obtained from a rabbit immunized with the mitochondrial tryparedoxin peroxidase recombinant protein. All the tested ferrocenyl diamine hydrochlorides were more cytotoxic than benznidazole. The expression of the 25.5 kDa polypeptide of mitochondrial tryparedoxin peroxidase did not increase in strains that were more resistant to the ferrocenyl compounds (SI8 and SIGR3). In addition, a 58 kDa polypeptide was also recognized in all strains. Ferrocenyl diamine hydrochlorides showed trypanocidal activity and the expression of 25.5 kDa mitochondrial tryparedoxin peroxidase is not necessarily increased in some T. cruzi strains. Most likely, other mechanisms, in addition to the over expression of this antioxidative enzyme, should be involved in the escape of parasites from cytotoxic oxidant agents.
Descritores: Peroxidases/metabolismo
Compostos Ferrosos/farmacologia
Proteínas de Protozoários/metabolismo
Oxidantes/farmacologia
Diaminas/farmacologia
Mitocôndrias/enzimologia
-Trypanosoma cruzi/efeitos dos fármacos
Trypanosoma cruzi/enzimologia
Western Blotting
Mitocôndrias/efeitos dos fármacos
Limites: Animais
Gatos
Coelhos
Responsável: BR1.1 - BIREME


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Id: biblio-1019501
Autor: Wang, Wenting; Zhu, Mingyue; Xu, Zhixin; Li, Wei; Dong, Xu; Chen, Yi; Lin, Bo; Li, Mengsen.
Título: Ropivacaine promotes apoptosis of hepatocellular carcinoma cells through damaging mitochondria and activating caspase-3 activity
Fonte: Biol. Res;52:36, 2019. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Natural Science Foundation of Hainan Province; . Undergraduate Student Innovate Project of Hainan Medical College.
Resumo: BACKGROUND: Recent evidences indicated that some local anaesthetic agents played a role in inhibiting the proliferation of cancer cells; Whether ropivacaine is able to promote apoptosis of hepatocellular carcinoma (HCC) cells is still unclear. The aim of this study was to investigate the effect of ropivacaine on the apoptosis of HCC cells. METHODS: In the present study, we treated the HCC cell lines, Bel7402 and HLE with ropivacaine. MTT, DAPI stain, trypan blue exclusion dye assay, flow cytometry, electron microscopy, computational simulation, laser confocal microscope, Western blotting, and enzyme activity analysis of caspase-3 were applied to detect the growth and apoptosis of HCC cells and to explore the role mechanism of ropivacaine. RESULTS: Ropivacaine was able to inhibit proliferation and promote apoptosis of HCC cells in a dose- and time-dependent manner. Ropivacaine also has a trait to inhibit the migration of HCC cells; ropivacaine damaged the mitochondria of HCC cells. The results also indicated that ropivacaine was able to interact with caspase-3, promote cytoplasmic caspase-3 migration into the nucleus, stimulate cleavage of caspase-3 and PARP-1, caspase-9 proteins, inhibit the expression of Bcl-2, promote expression of Apaf-1 and mitochondria release cytochrome C, and activate the activity of caspase-3. CONCLUSIONS: Ropivacaine has a novel role in promoting apoptosis of HCC cells; The role mechanism of ropivacaine maybe involve in damaging the function of mitochondria and activating the caspase-3 signalling pathway in HCC cells. Our findings provide novel insights into the local anaesthetic agents in the therapy of HCC patients.
Descritores: Apoptose/efeitos dos fármacos
Carcinoma Hepatocelular/patologia
Caspase 3/metabolismo
Ropivacaina/farmacologia
Anestésicos Locais/farmacologia
Neoplasias Hepáticas/patologia
-Transdução de Sinais/efeitos dos fármacos
Apoptose/fisiologia
Carcinoma Hepatocelular/metabolismo
Microscopia Confocal
Linhagem Celular Tumoral
Proliferação de Células/efeitos dos fármacos
Citometria de Fluxo
Neoplasias Hepáticas/metabolismo
Microscopia de Fluorescência
Mitocôndrias/efeitos dos fármacos
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1019509
Autor: Lu, Jinsen; Yang, Jiazhao; Zheng, Yongshun; Fang, Shiyuan; Chen, Xiaoyu.
Título: Resveratrol reduces store-operated Ca2+ entry and enhances the apoptosis of fibroblast-like synoviocytes in adjuvant arthritis rats model via targeting ORAI1-STIM1 complex
Fonte: Biol. Res;52:45, 2019. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: BACKGROUND: Resveratrol was reported to trigger the apoptosis of fibroblast-like synoviocytes In adjuvant arthritis rats but the subcellular mechanism remains unclear. Since ER stress, mitochondrial dysfunction and oxidative stress were involved in the effects of resveratrol with imbalance of calcium bio-transmission, store operated calcium entry (SOCE), a novel intracellular calcium regulatory pathway, may also participate in this process. RESULTS: In the present study, Resveratrol was found to suppress ORAI1 expression of a dose dependent manner while have no evident effects on STIM1 expressive level. Besides, resveratrol had no effects on ATP or TG induced calcium depletion but present partly dose-dependent suppression of SOCE. On the one hand, microinjection of ORAI1 overexpressed vector in sick toe partly counteracted the therapeutic effects of resveratrol on adjuvant arthritis and serum inflammatory cytokine including IL-1, IL-6, IL-8, IL-10 and TNF-α. On the other hand, ORAI1 SiRNA injection provided slight relief to adjuvant arthritis in rats. In addition, ORAI1 overexpression partly diminished the alleviation of hemogram abnormality induced by adjuvant arthritis after resveratrol treatment while ORAI1 knockdown presented mild resveratrol-like effect on hemogram in rats model. CONCLUSION: These results indicated that resveratrol reduced store-operated Ca2+ entry and enhanced the apoptosis of fibroblast-like synoviocytes in adjuvant arthritis rats model via targeting ORAI1-STIM1 complex, providing a theoretical basis for ORAI1 targeted therapy in future treatment with resveratrol on rheumatoid arthritis.
Descritores: Artrite Experimental/fisiopatologia
Canais de Cálcio/efeitos dos fármacos
Apoptose/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Sinoviócitos/efeitos dos fármacos
Molécula 1 de Interação Estromal/efeitos dos fármacos
Proteína ORAI1/efeitos dos fármacos
Resveratrol/farmacologia
-Canais de Cálcio/fisiologia
Estresse Oxidativo/efeitos dos fármacos
Resveratrol/administração & dosagem
Mitocôndrias/efeitos dos fármacos
Limites: Animais
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1124213
Autor: Zhao, Xiaoying; Zhang, Erfei; Ren, Xiaofen; Bai, Xiaoli; Wang, Dongming; Bai, Ling; Luo, Danlei; Guo, Zheng; Wang, Qiang; Yang, Jianxin.
Título: Edaravone alleviates cell apoptosis and mitochondrial injury in ischemia-reperfusion-induced kidney injury via the JAK/STAT pathway
Fonte: Biol. Res;53:28, 2020. graf.
Idioma: en.
Projeto: Health commission of Shanxi province.
Resumo: BACKGROUND: Kidney ischemia-reperfusion injury is a common pathophysiological phenomenon in the clinic. A large number of studies have found that the tyrosine protein kinase/signal transducer and activator of transcription (JAK/STAT) pathway is involved in the development of a variety of kidney diseases and renal protection associated with multiple drugs. Edaravone (EDA) is an effective free radical scavenger that has been used clinically for the treatment of postischemic neuronal injury. This study aimed to identify whether EDA improved kidney function in rats with ischemia-reperfusion injury by regulating the JAK/STAT pathway and clarify the underlying mechanism. METHODS: Histomorphological analysis was used to assess pathological kidney injury, and mitochondrial damage was observed by transmission electron microscopy. Terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL) staining was performed to detect tubular epithelial cell apoptosis. The expression of JAK2, P-JAK2, STAT3, P-STAT3, STAT1, P-STAT1, BAX and Bcl-2 was assessed by western blotting. Mitochondrial function in the kidney was assessed by mitochondrial membrane potential (ΔψM) measurement. RESULTS: The results showed that EDA inhibited the expression of p-JAK2, p-STAT3 and p-STAT1, accompanied by downregulation of the expression of Bax and caspase-3, and significantly ameliorated kidney damage caused by ischemia-reperfusion injury (IRI). Furthermore, the JC-1 dye assay showed that edaravone attenuated ischemia-reperfusion-induced loss of kidney (ΔψM). CONCLUSION: Our findings indicate that EDA protects against kidney damage caused by ischemia-reperfusion through JAK/STAT signaling, inhibiting apoptosis and improving mitochondrial injury.
Descritores: Traumatismo por Reperfusão/tratamento farmacológico
Depuradores de Radicais Livres/farmacologia
Edaravone/farmacologia
-Transdução de Sinais/efeitos dos fármacos
Ratos Sprague-Dawley
Apoptose
Fatores de Transcrição STAT/efeitos dos fármacos
Janus Quinases/efeitos dos fármacos
Mitocôndrias
Limites: Animais
Masculino
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: lil-691497
Autor: Mesquita, Juliana Tonini.
Título: Mecanismo de ação de fármacos sintéticos e associações terapêuticas em Leishmania (L) infantum / Mechanism of action of synthetic drugs and therapeutic associations in Leishmania (L) infantum.
Fonte: São Paulo; s.n; 2013. 105 p. ilus, tab.
Idioma: pt.
Tese: Apresentada a São Paulo(Estado) Secretaria da Saúde. Coordenadoria de Controle de Doenças. Programa de Pós Graduação em Ciências para obtenção do grau de Mestre.
Resumo: A leishmaniose visceral (LV) é uma doença negligenciada endêmica em 68 países e que se tornou um grande problema na área da saúde pública. Essa doença afeta principalmente populações menos favorecidas, onde o acesso, os cuidados médicos e a terapia medicamentosa são limitados. Visando buscar novas alternativas para o tratamento da LV, o reposicionamento de fármacos oferece uma grande oportunidade para introdução de novas terapias. Por meio desta abordagem, foi realizada em Leishmania (Leishmania) infantum: i) a triagem de oito fármacos nitrogenados, sendo eles: bifonazol, clotrimazol, cloxazolam, econazol, hidroxizina, loratadina, nitazoxanida e quetiapina; ii) o estudo da ação letal dos fármacos loratadina e nitazoxanida, e iii) o estudo in vitro da associação do fármaco nitazoxanida com fármacos padrões. Para isto, os possíveis mecanismos de ação foram estudados por meio de ensaios fluorimétricos, visando avaliar alteração de permeabilidade de membrana plasmática, alteração do potencial de membrana mitocondrial, produção de espécies reativas de oxigênio, exposição de fosfatidilserina, assim como o estudo das alterações ultraestruturais. Os resultados mostram que todos os fármacos apresentaram atividade contra formas promastigotas, com concentração efetiva 50% (CE50) entre 2 e 167 μM; apenas o econazol e a nitazoxanida eliminaram os amastigotas intracelulares, com CE50 de 11 a 22 μM, respectivamente. O fármaco loratadina alterou a permeabilidade da membrana plasmática do parasita, causando poros e levando o parasita a morte. O estudo da ação letal da nitazoxanida em Leishmania sugere que o fármaco tenha como alvo a mitocôndria, considerando a despolarização do potencial de membrana mitocondrial e aumento da produção de espécies reativas de oxigênio, resultando em estresse oxidativo e morte celular. Além disso, a presença de marcadores específicos como a exposição de fosfatidilserina e alterações...
Descritores: Farmacologia
Leishmania
Mitocôndrias
Preparações Farmacêuticas
Reposicionamento de Medicamentos
Terapêutica
Responsável: BR76.1 - Biblioteca
BR91.2; W4, M582m


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Id: biblio-871094
Autor: Corrêa, Daniela Saraiva.
Título: Estudo das alterações bioenergéticas induzidas por compostos sintéticos em Leishmania spp / Study of Bioenergetic Changes Induced by Synthetic Compounds in Leishmania spp.
Fonte: São Paulo; s.n; 2014. 152 p. ilus, map, tab, graf.
Idioma: pt.
Tese: Apresentada a São Paulo (Estado). Secretaria da Saúde. Coordenadoria e Controle de Doenças. Programa de Pós-Graduação em Ciências para obtenção do grau de Doutor.
Resumo: A leishmaniose é uma doença negligenciada, com especial incidência nos países em desenvolvimento; hoje em dia, 350 milhões de pessoas estão em risco de contrair esta doença, com 2 milhões de novos casos notificados anualmente. O tratamento é reduzido à quimioterapia, com uma escassez alarmante de medicamentos em uso clínico atual e diversos efeitos colaterais, além de relatos de resistência associados a muitos desses medicamentos. Todo esse contexto leva a necessidade da busca urgente de novos fármacos. Neste trabalho avaliou-se o potencial leishmanicida de 63 benzofenonas sintéticas, juntamente com o fármaco buparvaquona, uma naftoquinona usada atualmente para o tratamento da theileriose, sendo uma alternativa no estudo de reposicionamento de fármacos, sendo essa uma estratégia próspera e de baixo custo para a busca de novas drogas leishmanicidas...
Descritores: Fosforilação Oxidativa
Leishmaniose
Mitocôndrias
Sais
Transporte de Elétrons
Trifosfato de Adenosina
Responsável: BR91.2 - Centro de Documentação
BR91.2; W4, C824e, 2014



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