JOSE MARA DE BRITO

(Fonte: Lattes)
Índice h a partir de 2011
10
Projetos de Pesquisa
Unidades Organizacionais
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 10 de 12
  • article 18 Citação(ões) na Scopus
    Hematological changes and cytogenotoxicity in the tilapia Oreochromis niloticus caused by sub-chronic exposures to mercury and selenium
    (2015) SERIANI, Robson; FRANCA, Jakeline Galvao; LOMBARDI, Julio Vicente; BRITO, Jose Mara; RANZANI-PAIVA, Maria Jose Tavares
    Fish bioassays are valuable tools that can be used to elucidate the toxicological potential of numerous substances that are present in the aquatic environment. In this study, we assessed the antagonistic action of selenium (Se) against the toxicity of mercury (Hg) in fish (Oreochromis niloticus). Six experimental groups with six fish each were defined as follows: (1) control, (2) mercury (HgCl2), (3) sodium selenite (Na2Se4O3), (4) sodium selenate (Na2Se6O4), (5) mercury + sodium selenite (HgCl2 + Na2Se4O3), and (6) mercury + sodium selenate (HgCl2 + Na2Se6O4). Hematological parameters [red blood cells (RBC), white blood cells (WBC), and erythroblasts (ERB)] in combination with cytogenotoxicity biomarkers [nuclear abnormalities (NAs) and micronuclei (MN)] were examined after three, seven, ten, and fourteen days. After 7 days of exposure, cytogenotoxic effects and increased erythroblasts caused by mercury, leukocytosis triggered by mercury + sodium selenite, leukopenia associated with sodium selenate, and anemia triggered by mercury + sodium selenate were observed. Positive correlations that were independent of time were observed between WBC and RBC, ERB and MN, and NA and MN. The results suggest that short-term exposure to chemical contaminants elicited changes in blood parameters and produced cytogenotoxic effects. Moreover, NAs are the primary manifestations of MN formation and should be included in a class characterized as NA only. Lastly, the staining techniques used can be applied to both hematological characterization and the measurement of cytogenotoxicity biomarkers.
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    Time-dependent effects of diesel exhaust exposure on worsening of emphysema
    (2017) MOREIRA, Alyne Riani; LOURENCO, Juliana D.; KOHLER, Julia B.; EMIDIO, Larissa; CASTRO, Thamyres; DELESPOSTE, Luciano; SARAIVA, Beatriz M.; BRITO, Jose Mara; OLIVO, Clarice; PRADO, Carla M.; MARTINS, Milton; LOPES, Fernanda D. T. Q. S.; RIVERO, Dolores
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    Effects of air pollution on inflammation of respiratory system: Differences between male and female
    (2015) YOSHIZAKI, Kelly; LINO-DOS-SANTOS-FRANCO, Adriana; BRITO, Jose Mara; SANTOS, Thais Moraes Nascimento; VASCONCELOS, Perola; MAUAD, Thais; SALDIVA, Paulo Hilario Nascimento; MACCHIONE, Mariangela
  • article 10 Citação(ões) na Scopus
    Enriched inorganic compounds in diesel exhaust particles induce mitogen-activated protein kinase activation, cytoskeleton instability, and cytotoxicity in human bronchial epithelial cells
    (2015) SERIANI, Robson; JUNQUEIRA, Mara S.; CARVALHO-SOUSA, Claudia E.; ARRUDA, Alessandra Ct.; MARTINEZ, Diana; ALENCAR, Adriano M.; GARIPPO, Ana L.; BRITO, Jose Mara; MARTINS, Milton A.; SALDIVA, Paulo H. N.; NEGRI, Elnara M.; MAUAD, Thais; MACCHIONE, Mariangela
    This study assessed the effects of the diesel exhaust particles on ERR and JNK MAPKs activation, cell rheology (viscoelasticity), and cytotoxicity in bronchial epithelial airway cells (BEAS-2B). Crude DEP and DEP after extraction with hexane (DEP/HEX) were utilized. The partial reduction of some DEP/HEX organics increased the biodisponibility of many metallic elements. JNK and ERR were activated simultaneously by crude DEP with no alterations in viscoelasticity of the cells. Mitochondrial activity, however, revealed a decrease through the MIT assay. DEP/HEX treatment increased viscoelasticity and cytotoxicity (membrane damage), and also activated JNK. Our data suggest that the greater bioavailability of metals could be involved in JNK activation and, consequently, in the reduction of fiber coherence and increase in the viscoelasticity and cytotoxicity of BEAS cells. The adverse findings detected after exposure to crude DEP and to DEP/HEX reflect the toxic potential of diesel compounds. Considering the fact that the cells of the respiratory epithelium are the first line of defense between the body and the environment, our data contribute to a better understanding of the pathways leading to respiratory cell injury and provide evidence for the onset of or worsening of respiratory diseases caused by inorganic compounds present in DEP.
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    The effects of concentrated air pollution by gender: Experimental study in mice
    (2014) YOSHIZAKI, Kelly; FUZIWARA, Cesar S.; BRITO, Jose Mara; SANTOS, Thais M. N.; KIMURA, Edna T.; CORREIA, Aristides T.; VASCONCELOS, Perola; SILVA, Luiz F. F.; MAUAD, Thais; SALDIVA, Paulo H. N.; MACCHIONE, Mariangela
  • article 22 Citação(ões) na Scopus
    Chronic exposure of diesel exhaust particles induces alveolar enlargement in mice
    (2015) YOSHIZAKI, Kelly; BRITO, Jose Mara; MORIYA, Henrique T.; TOLEDO, Alessandra C.; FERZILAN, Sandra; OLIVEIRA, Ana Paula Ligeiro de; MACHADO, Isabel D.; FARSKY, Sandra H. P.; SILVA, Luiz F. F.; MARTINS, Milton A.; SALDIVA, Paulo H. N.; MAUAD, Thais; MACCHIONE, Mariangela
    Background: Diesel exhaust particles (DEPs) are deposited into the respiratory tract and are thought to be a risk factor for the development of diseases of the respiratory system. In healthy individuals, the timing and mechanisms of respiratory tract injuries caused by chronic exposure to air pollution remain to be clarified. Methods: We evaluated the effects of chronic exposure to DEP at doses below those found in a typical bus corridor in Sao Paulo (150 mu g/m(3)). Male BALB/c mice were divided into mice receiving a nasal instillation: saline (saline; n = 30) and 30 mu g/10 mu L of DEP (DEP; n = 30). Nasal instillations were performed five days a week, over a period of 90 days. Bronchoalveolar lavage (BAL) was performed, and the concentrations of interleukin (IL)-4, IL-10, IL-13 and interferon-gamma (INF-gamma) were determined by ELISA-immunoassay. Assessment of respiratory mechanics was performed. The gene expression of Muc5ac in lung was evaluated by RT-PCR. The presence of IL-13, MAC2+ macrophages, CD3+, CD4+, CD8+ T cells and CD20+ B cells in tissues was analysed by immunohistochemistry. Bronchial thickness and the collagen/elastic fibers density were evaluated by morphometry. We measured the mean linear intercept (Lm), a measure of alveolar distension, and the mean airspace diameter (D0) and statistical distribution (D2). Results: DEP decreased IFN-gamma levels in BAL (p = 0.03), but did not significantly alter IL-4, IL-10 and IL-13 levels. MAC2+ macrophage, CD4+ T cell and CD20+ B cell numbers were not altered; however, numbers of CD3+ T cells (p <= 0.001) and CD8+ T cells (p <= 0.001) increased in the parenchyma. Although IL-13 (p = 0.008) expression decreased in the bronchiolar epithelium, Muc5ac gene expression was not altered in the lung of DEP-exposed animals. Although respiratory mechanics, elastic and collagen density were not modified, the mean linear intercept (Lm) was increased in the DEP-exposed animals (p <= 0.001), and the index D2 was statistically different (p = 0.038) from the control animals. Conclusion: Our data suggest that nasal instillation of low doses of DEP over a period of 90 days results in alveolar enlargement in the pulmonary parenchyma of healthy mice.
  • article 34 Citação(ões) na Scopus
    The effects of particulate matter on inflammation of respiratory system: Differences between male and female
    (2017) YOSHIZAKI, Kelly; BRITO, Jose Mara; SILVA, Luiz Fernando; LINO-DOS-SANTOS-FRANCO, Adriana; FRIAS, Daniela Perroni; SILVA, Renata Calciolari Rossi e; AMATO-LOURENCO, Luis Fernando; SALDIVA, Paulo Hilario Nascimento; TIBERIO, Iolanda de Fatima Lopes Calvo; MAUAD, Thais; MACCHIONE, Mariangela
    Air pollution is known to exacerbate respiratory diseases and epidemiological studies have shown that women present more chronic respiratory symptoms than man exposed to traffic pollution, however, the reason why is unclear. This study evaluated the inflammatory differences in BALB/c mouse males (n = 34) and females (n = 111) in three phases of the estrous cycle that were exposed to ambient air (AA) or concentrated ambient particles (CAPs). Tracheal hyperreactivity to methacholine, bronchoalveolar lavage fluid (BALF) and immunohistochemical of airways and lung parenchyma were studied. Hyperreactivity increased in CAPs-exposed female mice compared with AA-exposed mice in estrus (p < 0.05) and proestrus phases (p < 0.05) and decreased in CAPs-exposed males compared with those exposed to AA (p < 0.05). Males had increased numbers of total cells (p = 0.037) and macrophages (p = 0.028) compared to females. BALF levels of cyclooxygenase-2(COX-2) (p = 0.000), transforming growth factor alpha (TGF-alpha) (p = 0.001) and IL-8 receptor alpha (IL-8R alpha) (p = 0.014) were increased in males compared with proestrus, estrus and diestrus females, independent of exposure. Proestrus females exhibited significantly higher cadherin expression in lung parenchyma than did males (p = 0.005). CAPs exposure increased matrix metalloproteinase-9 (MMP-9) (p = 0.024) and isoprostane (p = 0.003) expression in the airways of both, males and females. The level of substance P (SP) (p = 0.001) increased in lung parenchyma in males compared with females, while IL-17 levels in airways (p = 0.042) and in lung parenchyma (p = 0.008) increased in females. MMP-9 levels (p = 0.024) were significantly lower in the lung parenchyma of CAPs-exposed females. TGF-alpha (p = 0.007) levels increased in the lung parenchyma of CAPs-exposed females compared to AA-exposed females. These results suggest that inflammatory markers differentially expressed in male mice were mostly linked to acute inflammation (IL-1 beta, IL-8R alpha, COX-2), whereas in females, markers that may lead to a chronic inflammatory process such as IL-17 and remodeling (MMP-9) were increased.
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    Inhalation of exhaust particles of biodiesel fuel promotes similar alterations on heart rate variability induced by diesel fuel
    (2014) MACCHIONE, Mariangela; BRITO, Jose Mara; CAVALHEIRO, Guilherme; YOSHIZAKI, Kelly; GUIMARAES, Eliane; LICHTENFELS, Ana Julia; ANDRE, Paulo; RIVERO, Dolores; SALDIVA, Paulo
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    Gender differences in the pulmonary acute inflammatory response to concentrated ambient particles in mice
    (2012) YOSHIZAKI, Kelly; BRITO, Jose Mara; SANTOS, Thais Moraes do Nascimento; SALDIVA, Paulo Hilario Nascimento; SILVA, Luiz Fernando Ferraz da; MAUAD, Thais; MACCHIONE, Mariangela
  • article 5 Citação(ões) na Scopus
    Bronchial responsiveness in an elastase-induced mouse model of emphysema
    (2014) SANTOS, Luiz Marcelo Oliveira; CERVILHA, Daniela Aparecida de Brito; CABRAL, Layla Dutra Marinho; GARCIA, Erika Kristina Incerpi; TEIXEIRA, Vanessa Pereira; BRITO, Jose Mara; MORIYA, Henrique Takachi; SONCINI, Roseli
    Bronchial responsiveness during methacholine (MCh) challenge was analysed in an elastase-induced mouse model of emphysema to explore the magnitude of the response in this model. Swiss mice were intratracheally instilled with saline or elastase (0.3 or 0.6 U). Twenty days afterward, mechanical ventilation data were collected from the closed and opened thorax of baseline and MCh (vehicle, 50 and 100 mg/mL) challenged mice. The lungs were prepared for morphometric analysis. In the 0.6 U group, airway resistance (R-aw) and tissue elastance (H) were decreased, and hysteresivity (eta) was increased (closed thorax). MCh increased R-aw, G and H in all groups, but this increase was attenuated in the elastase-induced emphysema groups, the largest attenuation was observed in the 0.6 U (closed thorax condition). Elastase increased hyperinflation of the alveoli, alveolar collapse and the Lm and reduced the normal area. MCh reduced respiratory mechanics in elastase-induced emphysema, and this reduction was modulated by the collapsed and/or hyperinflated areas, which increased the heterogeneity of the lungs. Crown