Producción CyT
Artículo
Autoría
Cáceres, Lourdes
;
PAZ, MARIELA LAURA
;
Garcés, Mariana
;
Calabró López, María Valeria
;
MAGNANI, NATALIA DANIELA
;
Martinefski, Manuela
;
Martino Adami, Pamela Victoria
;
CALTANA, LAURA ROMINA
;
Tasat, Deborah
;
MORELLI, LAURA
;
TRIPODI, VALERIA PAULA
;
Valacchi, Giuseppe
;
ALVAREZ, SILVIA
;
GONZALEZ MAGLIO, DANIEL HORACIO
;
Marchini, Timoteo Oscar
;
EVELSON, PABLO ANDRES
Fecha
2020
Editorial y Lugar de Edición
ACADEMIC PRESS INC ELSEVIER SCIENCE
Revista
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY,
vol. 205
(pp. 1-13)
ACADEMIC PRESS INC ELSEVIER SCIENCE
Resumen
Información suministrada por el agente en
SIGEVA
Exposure to ambient air particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality. In this context, alveolar macrophages exhibit proinflammatory and oxidative responses as a result of the clearance of particles, thus contributing to lung injury. However, the mechanisms linking these pathways are not completely clarified. Therefore, the oxinflammation phenomenon was studied in RAW 264.7 macrophages exposed to Residual Oil Fly Ash (ROFA), a PM surrogate rich i...
Exposure to ambient air particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality. In this context, alveolar macrophages exhibit proinflammatory and oxidative responses as a result of the clearance of particles, thus contributing to lung injury. However, the mechanisms linking these pathways are not completely clarified. Therefore, the oxinflammation phenomenon was studied in RAW 264.7 macrophages exposed to Residual Oil Fly Ash (ROFA), a PM surrogate rich in transition metals. While cell viability was not compromised under the experimental conditions, a proinflammatory phenotype was observed in cells incubated with ROFA 100 ?g/mL, characterized by increased levels of TNF-? and NO production, together with PM uptake. This inflammatory response seems to precede alterations in redox metabolism, characterized by augmented levels of H2O2, diminished GSH/GSSG ratio, and increased SOD activity. This scenario resulted in increased oxidative damage to phospholipids. Moreover, alterations in mitochondrial respiration were observed following ROFA incubation, such as diminished coupling efficiency and spare respiratory capacity, together with augmented proton leak. These findings were accompanied by a decrease in mitochondrial membrane potential. Finally, NADPH oxidase (NOX) and mitochondria were identified as the main sources of superoxide anion ([Formula presented]) in our model. These results indicate that PM exposure induces direct activation of macrophages, leading to inflammation and increased reactive oxygen species production through NOX and mitochondria, which impairs antioxidant defense and may cause mitochondrial dysfunction.
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Palabras Clave
MACROPHAGESINFLAMMATIONOXIDATIVE STRESSAIR POLLUTIONNADPH OXIDASEMITOCHONDRIA
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