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Vanadium pentoxide induces activation and death of endothelial cells
Author(s) -
MontielDávalos Angélica,
GonzalezVillava Adriana,
RodriguezLara Vianey,
Montaño Luis Felipe,
Fortoul Teresa I.,
LópezMarure Rebeca
Publication year - 2012
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1695
Subject(s) - vanadium , pentoxide , chemistry , microbiology and biotechnology , biophysics , biology , inorganic chemistry
ABSTRACT Vanadium is a transition metal released into the atmosphere, as air‐suspended particles, as a result of the combustion of fossil fuels and some metallurgic industry activities. Air‐suspended particle pollution causes inflammation‐related processes such as thrombosis and other cardiovascular events. Our aim was to evaluate the effect of vanadium pentoxide (V 2 O 5 ) on endothelial cells since they are key participants in the pathogenesis of several cardiovascular and inflammatory diseases. Cell adhesion, the expression of adhesion molecules and oxidative stress, as well as proliferation, morphology and cell death of human umbilical vein endothelial cells (HUVECs) exposed to V 2 O 5 , were evaluated. Vanadium pentoxide at a 3.12 µg cm −2 concentration induced an enhanced adhesion of the U937 macrophage cell line to HUVECs, owing to an increased expression of late adhesion molecules. HUVECs exposed to V 2 O 5 showed an increase in ROS and nitric oxide production, and a diminished proliferation. These changes in vanadium‐treated HUVECs were accompanied by severe morphological changes and apoptotic cell death. Vanadium pentoxide induced serious endothelial cell damage, probably related to the increased cardiovascular morbidity and mortality observed in individuals living in highly air‐polluted areas. Copyright © 2011 John Wiley & Sons, Ltd.