RESUMEN
Determinou-se a concentração eficaz de oxitetraciclina (OTC) e florfenicol (FFC) no tratamento de Aeromonas hydrophila em pacu (Piaractus. mesopotamicus). Os pacus foram submetidos à captura duas vezes ao dia por quatro dias e em seguida foram infectados com A. hydrophila (2,4x10(7) bactéria mL-1). Os tratamentos utilizados foram: controle sem infecção (CSI), controle com infecção (CCI) e tratados com 110,0; 140,0 e 170,0mgOTC.kg-1, e 5,0; 10,0 e 15,0mgFFC.kg-1. As variáveis de qualidade da água foram monitoradas diariamente. Após o tratamento, no CSI dos dois testes, ocorreu 100 por cento de sobrevivência. Nos testes com OTC, no CCI, a sobrevivência foi de 29,2 por cento; em 110,0mg.kg-1, 37,5 por cento; em 140,0mg.kg-1, 29,2 por cento; e em 170,0mg.kg-1, 50,0 por cento. Nos testes com FFC, foi eficaz com 10,0mg.kg-1, e no CCI a sobrevivência foi de 76,9 por cento; em 5,0mg.kg-1, 81,81 por cento; em 10,0mg/L.kg-1, 100 por cento e em 15,0mg.kg-1, 87,5 por cento. A OTC, em concentrações de até 170,0mg.kg-1 de ração, não é eficaz para o controle de A. hydrophila em pacu, e o FFC é eficaz na concentração de 10,0mg.kg-1 e ambos não alteram as variáveis de qualidade de água.
The effective concentration of antibiotics OTC and FFC in the treatment of Aeromonas hydrophila in pacu (Piaractus mesopotamicus). The pacus were subjected to capture twice daily (four days) and then were infected with A. hydrophila (2.4 x10 7 bacteria mL -1 ). The treatments were: control without infection (CSI), with infection control (CCI) and 110.0, 140.0 and 170.0mgOTC.kg -1 , and 5.0, 10.0 and 15.0mgFFC.kg -1 . The variables of water quality were monitored daily. After treatment, the CSI of the two experiments was 100 percent survival. In tests with OTC, the CCI was 29.17 percent, in 110.0mg.kg -1 , 37.5 percent, in 140.0mg.kg -1 , 29.17 percent and in 170.0mg.kg -1 , 50.0 percent. The FFC was effective with 10.0 mg kg -1 , and in the CCI the survival was 76.9 percent, in 5.0mg.kg -1 , 81.81 percent, in 10.0mg/L.kg -1 , 100 percent and in 15.0mg.kg -1 , 87.5 percent. The OTC in concentrations of up to 170.0 mg.kg -1 of ration is not effective in the control of A. hydrophila in pacu and the FFC is effective in the concentration of 10.0mg.kg -1 and this antibiotic does not change the variables of water quality.
Asunto(s)
Animales , Antibacterianos , Aeromonas hydrophila/inmunología , Peces/parasitologíaRESUMEN
Interleukin-7 (IL-7) activates phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway, thereby mediating viability, proliferation and growth of T-cell acute lymphoblastic leukemia (T-ALL) cells. Reactive oxygen species (ROS) can be upregulated by growth factors and are known to regulate proliferation and viability. Here, we show that IL-7 upregulates ROS in T-ALL cells in a manner that is dependent on PI3K/Akt/mTOR pathway activity and that relies on both NADPH oxidase and mitochondrial respiratory chain. Conversely, IL-7-induced activation of PI3K signaling pathway requires mitochondrial respiration and ROS. We have previously shown that IL-7-mediated activation of PI3K pathway drives the upregulation of the glucose transporter Glut1, promoting glucose uptake in T-ALL cells. Using phloretin to inhibit Glut function, we demonstrate that glucose uptake is mandatory for ROS upregulation in IL-7-treated T-ALL cells, suggesting that IL-7 stimulation leads to increased ROS via PI3K pathway activation and consequent upregulation of Glut1 and glucose uptake. Overall, our data reveal the existence of a critical crosstalk between PI3K/Akt signaling pathway and ROS that is essential for IL-7-mediated T-ALL cell survival, and that may constitute a novel target for therapeutic intervention.
Asunto(s)
Supervivencia Celular , Interleucina-7/fisiología , Leucemia-Linfoma Linfoblástico de Células T Precursoras/patología , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal/fisiología , Proliferación Celular , Humanos , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Receptor Cross-Talk , Serina-Treonina Quinasas TOR/metabolismo , Células Tumorales Cultivadas , Regulación hacia ArribaRESUMEN
T-cell acute lymphoblastic leukemia (T-ALL) is a biologically heterogeneous disease with respect to phenotype, gene expression profile and activation of particular intracellular signaling pathways. Despite very significant improvements, current therapeutic regimens still fail to cure a portion of the patients and frequently implicate the use of aggressive protocols with long-term side effects. In this review, we focused on how deregulation of critical signaling pathways, in particular Notch, PI3K/Akt, MAPK, Jak/STAT and TGF-beta, may contribute to T-ALL. Identifying the alterations that affect intracellular pathways that regulate cell cycle and apoptosis is essential to understanding the biology of this malignancy, to define more effective markers for the correct stratification of patients into appropriate therapeutic regimens and to identify novel targets for the development of specific, less detrimental therapies for T-ALL.
Asunto(s)
Diferenciación Celular , Leucemia-Linfoma de Células T del Adulto , Fosfotransferasas/fisiología , Transducción de Señal/fisiología , Linfocitos T/citología , Humanos , Quinasas Janus/fisiología , Leucemia-Linfoma de Células T del Adulto/etiología , Leucemia-Linfoma de Células T del Adulto/fisiopatología , Leucemia-Linfoma de Células T del Adulto/terapia , Proteínas Quinasas Activadas por Mitógenos/fisiología , Fosfatidilinositol 3-Quinasas/fisiología , Fosforilación , Proteínas Proto-Oncogénicas c-akt/fisiología , Receptores Notch/fisiología , Factor de Crecimiento Transformador beta/fisiologíaRESUMEN
T-cell acute lymphoblastic leukemia (T-ALL) is a biologically heterogeneous disease with respect to phenotype, gene expression profile and activation of particular intracellular signaling pathways. Despite very significant improvements, current therapeutic regimens still fail to cure a portion of the patients and frequently implicate the use of aggressive protocols with long-term side effects. In this review, we focused on how deregulation of critical signaling pathways, in particular Notch, PI3K/Akt, MAPK, Jak/STAT and TGF-ß, may contribute to T-ALL. Identifying the alterations that affect intracellular pathways that regulate cell cycle and apoptosis is essential to understanding the biology of this malignancy, to define more effective markers for the correct stratification of patients into appropriate therapeutic regimens and to identify novel targets for the development of specific, less detrimental therapies for T-ALL.