Browsing by Subject "Vanadium"

Now showing 1 - 3 of 3
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    Sex differences in vanadium inhalation effects in non-ciliated bronchiolar cells
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) López Valdez, Nelly; Rojas Lemus, Marcela; Bizarro Nevares, Martha Patricia; González Villalva, Adriana Elizabeth; Ustarroz Cano, Martha Luz; Casarrubias Tabarez, Brenda; Guerrero Palomo, Gabriela; Cervantes Valencia, María Eugenia; Rivera Fernández, Norma; Imelda Fortoul, Teresa
    The non-ciliated bronchiolar cell (NCBC) is responsible for the defense of the lung and responds to negative stimuli such as exposure to toxic pro-oxidant substances, which triggers the hyperproduction and hypersecretion of mucins and CC16 protein. The literature demonstrates that physiological and pathological responses in the lung can be influenced by the organism’s sex. The objective of this report was to evaluate response differences to vanadium inhalation in male and female CD-1 mice. Mice were exposed to vanadium for four weeks. Hyperplasia of bronchiolar epithelium, small inflammatory foci and sloughing of the NCBC were observed, without changes between sexes and throughout the exposure time. Mucosecretory metaplasia was found in both males and females, however it was more drastic in males. The expression of CC16 increased in both sexes. This study demonstrated a different susceptibility between male and female mice exposed to vanadium inhalation regarding mucosecretory metaplasia.
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    Spleen and bone marrow megakaryocytes as targets for inhaled vanadium
    (Murcia : F. Hernández, 2008) Fortoul, Teresa I.; Piñón-Zarate, Gabriela; Diaz-Bech, María Eugenia; González-Villalva, Adriana; Mussali-Galante, Patricia; Rodriguez-Lara,Vilaney; Colin-Barenque, Laura; Martinez Pedraza, Michelle; Montaño, Luis F.
    An increased incidence in ischemic and thromboembolic events in the population of cities with rising air suspended particle pollution has suggested the interaction of some of the components of these particles in the coagulation system. A previous report from our laboratory identified thrombocytosis as a consequence of the subacute and chronic inhalation of vanadium. With this preceding information we decided to evaluate the effects of this element in the spleen and bone marrow in a mouse experimental model. CD-1 male mice inhaled V2O5 0.02 M for one hour twice a week for twelve weeks. The spleen and bone marrow were processed for light microscopy. The increase in quantity and size of megakaryocytes (MKs) in the exposed group in both organs was striking. Also, modifications in the cytoplasm, granule content and nuclear ultrastructure were evident. Our results indicate the influence of vanadium on megakaryopoyesis, an effect which could be the onset of the thrombocytosis previously reported by our group. The modifications in MKs described here suggest that inhaled vanadium could induce megakaryocytic proliferation, which may result in increased production of platelets and increased risk for thromboembolic events.
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    The role of the non-ciliated bronchiolar cell in tolerance to inhaled vanadium of the bronchiolar epithelium
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) López Valdez, Nelly; Guerrero Palomo, Gabriela; Rojas-Lemus, Marcela; Bizarro-Nevares, Patricia; González-Villalva, Adriana; Ustarroz-Cano, Martha; Rivera-Fernández, Norma; Fortoul, Teresa I.
    The Non-Ciliated Bronchiolar Cell (NCBC) is responsible for the defense and maintenance of the bronchiolar epithelium. Several cellular defense mechanisms have been associated with an increase in the secretion of CC16 and changes in the phenotype of the cell; these mechanisms could be linked to tolerance to the damage due to exposure to inhaled Particulate Matter (PM) of the epithelium. These defense mechanisms have not been sufficiently explored. In this article, we studied the response of the NCBC to inhaled vanadium, an element which adheres to PM. This response was measured by the changes in the phenotype of the NCBC and the secretion of CC16 in a mouse model. Mice were exposed in two phases to different vanadium concentrations; 1.56 mg/m 3 in the first phase and 2.57 mg/m3 in the second phase. Mice were sacrificed on the 2nd, 4th, 5th, 6th and 8th weeks. In the second phase, we observed the following: sloughing of the NCBC, hyperplasia and small inflammatory foci remained without changes and that the expression of CC16 was higher in this phase than in phase I. We also observed a change in the phenotype with a slow decrease in both phases. The increase in the secretion of CC16 and the phenotype reversion could be due to the anti- inflammatory activity of CC16. The changes observed in the second phase could be attributed to the tolerance to inhaled vanadium.