Letts R.E.,Grande Rio University |
Letts R.E.,Cayetano Heredia Peruvian University |
Pereira T.C.B.,Grande Rio University |
Bogo M.R.,Grande Rio University |
And 3 more authors.
Archives of Environmental Contamination and Toxicology | Year: 2011
Bacteria communities living in mucus secretions of common carp Cyprinus carpio (Cyprinidae) were exposed to the organic nanomaterial fullerene (C 60) to evaluate its potential bactericidal effects. End points analyzed were viability, growth, reactive oxygen species (ROS) concentration, and total antioxidant competence against peroxyl radicals. Viability was not affected (p > 0.05), whereas growth was arrested (p < 0.05) after 3 hours of exposure to the three concentration of C 60 assayed (0.1, 1, and 10 mg/L). Levels of RO measured at different C 60 concentration showed that some colonies were reactive (significant dose-response relation, p < 0.05) to C 60, whereas others were not. The nonreactive colonies to C 60 presented higher antioxidant competence to peroxyl radicals compared with the reactive colonies (p < 0.05). The strains isolated and identified by polymerase chain reaction (PCR) products of 16S rRNA showed a predominance of Aeromonas genus between all the isolated Gram-negative bacteria. Thus, the present results indicate that C 60 affects bacterial communities that live in mucus secretions of common carp. © 2010 Springer Science+Business Media, LLC. Source
Izetti P.,Federal University of Rio Grande do Sul |
Izetti P.,Laboratorio Of Medicina Genomica |
Hautefeuille A.,International Agency for Research on Cancer |
Abujamra A.L.,Instituto Do Cancer Infantil Do Rio Grande Do sul |
And 11 more authors.
Investigational New Drugs | Year: 2014
TP53 mutation is a common event in many cancers, including pancreatic adenocarcinoma, where it occurs in 50-70 % of cases. In an effort to reactivate mutant p53 protein, several new drugs are being developed, including PRIMA-1 and PRIMA-1Met/APR-246 (p53 reactivation and induction of massive apoptosis). PRIMA-1 has been shown to induce apoptosis in tumor cells by reactivating p53 mutants, but its effect in pancreatic cancer remains unclear. Here we investigated the effects of PRIMA-1 on cell viability, cell cycle and expression of p53-regulated proteins in PANC-1 and BxPC-3 (mutant TP53), and CAPAN-2 (wild-type TP53) pancreatic cell lines. Treatment with PRIMA-1 selectively induced apoptosis and cell cycle arrest in p53 mutant cells compared to CAPAN-2 cells. The growth suppressive effect of PRIMA-1 was markedly reduced in p53 mutant cell lines transfected with p53 siRNA, supporting the role of mutant p53 in PRIMA-1 induced cell death. Moreover, treatment with the thiol group donor N-acetylcysteine completely blocked PRIMA-1-induced apoptosis and reinforced the hypothesis that thiol modifications are important for PRIMA-1 biological activity. In combination treatments, PRIMA-1 enhanced the anti-tumor activity of several chemotherapic drugs against pancreatic cancer cells and also exhibited a pronounced synergistic effect in association with the Mdm2 inhibitor Nutlin-3. Taken together, our data indicate that PRIMA-1 induces apoptosis in p53 mutant pancreatic cancer cells by promoting the re-activation of p53 and inducing proapoptotic signaling pathways, providing in vitro evidence for a potential therapeutic approach in pancreatic cancer. © 2014 Springer Science+Business Media New York. Source
Barichello T.,University of the Extreme South of Santa Catarina |
Fagundes G.D.,University of the Extreme South of Santa Catarina |
Generoso J.S.,University of the Extreme South of Santa Catarina |
Paula Moreira A.,University of the Extreme South of Santa Catarina |
And 8 more authors.
Brain Research | Year: 2012
Neonatal meningitis is an illness characterized by inflammation of the meninges and occurring within the birth and the first 28 days of life. Invasive infection by Streptococcus pneumoniae, meningitis and sepsis, in neonate is associated with prolonged rupture of membranes; maternal colonization/illness, prematurity, high mortality and 50% of cases have some form of disability. For this purpose, we measured brain levels of TNF-α, IL-1β, IL-6, IL-10, CINC-1, oxidative damage, enzymatic defense activity and the blood-brain barrier (BBB) integrity in neonatal Wistar rats submitted to pneumococcal meningitis. The cytokines increased prior to the BBB breakdown and this breakdown occurred in the hippocampus at 18 h and in the cortex at 12 h after pneumococcal meningitis induction. The time-dependent association between the complex interactions among cytokines, chemokine may be responsible for the BBB breakdown and neonatal pneumococcal severity. © 2012 Elsevier B.V. All rights reserved. Source
Da Cunha A.A.,Grande Rio University |
Pauli V.,Grande Rio University |
Saciura V.C.,Grande Rio University |
Constantino L.C.,University of the Extreme South of Santa Catarina |
And 11 more authors.
Chest | Year: 2010
Background: The aim of this study was to examine the effects of the N-methyl-D-aspartate receptor (NMDAR) channel blocker dizocilpine(MK-801) on lung injury in rats submitted to experimental sepsis induced by cecal ligation and perforation(CLP). Methods: Adult male Wistar rats submitted to CLP were given a single systemic injection of MK-801(subcutaneously at 0.3 mg/kg) administered 4 or 7 h after CLP induction. Twelve hours after CLP BAL was performed to determine total cell count, protein content, and inflammatory parameters. In addition, lung was excised for histopathologic analyses and determination of NMDAR subunits content. In a separate cohort of animals mortality was recorded for 5 days. Results: Animals submitted to sepsis induced by CLP showed an increase in the content of NMDAR subunits NR1 and NR2A in the lung. Administration of MK-801 4 h after CLP induction resulted in a decrease in BAL fluid cellular content and decreased levels of proinflammatory cytokines. In addition, MK-801 decreased lung oxidative stress markers and histopathologic alterations and improved survival. Conclusions: These findings indicate that NMDAR blockade might represent a promising novel therapeutic strategy for the treatment of sepsis and inflammatory disorders. © 2010 American College of Chest Physicians. Source
Biff D.,Instituto Nacional Of Ciencia E Tecnologia Translacional Em Medicina |
Petronilho F.,University of South Santa Catarina |
Constantino L.,Instituto Nacional Of Ciencia E Tecnologia Translacional Em Medicina |
Vuolo F.,Instituto Nacional Of Ciencia E Tecnologia Translacional Em Medicina |
And 6 more authors.
Shock | Year: 2013
Oxidative damage and inflammation occur early in the brain after sepsis and are resolved when long-term cognitive impairment occurs. There is no information of a direct relation between acute levels of brain inflammation and oxidative damage and long-term cognitive deficits. We hypothesized that higher levels of early oxidative damage and inflammation are followed by long-term cognitive deficits, and this is related to a decrease in the levels of brain-derived neurotropic factor (BDNF). Wistar rats were subjected to sham operation or cecal ligation and perforation and the cerebrospinal fluid (CSF) was obtained 6 and 24 h after the determination of thiobarbituric acidYreactive species, interleukin 1 (IL-1), IL-10, and tumor necrosis factor α (TNF-α). Animals were followed until 30 days after surgery and were subjected to the step-down inhibitory avoidance (IA) task, and the hippocampus levels of BDNF were determined. At 6 h, higher CSF levels of thiobarbituric acidYreactive species and TNF-α were observed in septic animals that had a better performance in the IA task and presented higher BDNF levels in the hippocampus. At 24 h, higher CSF levels of IL-1β and TNF-α were observed in septic animals that had a worse performance in the IA task, and this was associated with lower BDNF levels. The persistence of brain inflammation during the acute phase of sepsis is associated with long-term hippocampus levels of BDNF and memory impairment in sepsis survivors. © 2013 by the Shock Society. Source