Congreso
Autoría
Cáceres L
;
PAZ, MARIELA LAURA
;
Garcés M
;
Tasat D
;
González Maglio DH
;
Marchini T
;
Evelson PA
Fecha
2016
Editorial y Lugar de Edición
Estudio Sigma SRL
ISSN
0025-7680
Resumen
Información suministrada por el agente en
SIGEVA
The exposure to environmental particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality rates. Alveolar macrophages are suggested to play a central role in this scenario, triggering both inflammation and oxidative stress following PM inhalation. However, the pathways linking these responses remain uncertain. In order to address such mechanisms, we studied the murine macrophage cell line RAW 264.7 after an exposure to different PM samples, Residual Oil Fly As...
The exposure to environmental particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality rates. Alveolar macrophages are suggested to play a central role in this scenario, triggering both inflammation and oxidative stress following PM inhalation. However, the pathways linking these responses remain uncertain. In order to address such mechanisms, we studied the murine macrophage cell line RAW 264.7 after an exposure to different PM samples, Residual Oil Fly Ash (ROFA) and Concentrated Ambient Particles (CAPs),at 0, 50, 100, and 200 μg/mL for24 h. Intracellular redox status was assessed by dichlorofluorescein fluorescence, which was increased in a dose-dependent mannerby up to 73% and 71% at 200 μg/mLof ROFA and CAPs, respectively(control: 16 ± 5 (x103) AU, p<0.05).Oxidative damage to lipids was evaluated as thiobarbituric acid reactive substances (TBARS) by a fluorometric assay, finding a dose-dependent increase byup to 356% and 144% at 200 μg/mLof ROFA and CAPs, respectively(control: 0.29 ± 0.03 mmol TBARS/mg protein, p<0.01).Nitric oxide production was indirectly determined as nitrite content in cell culture supernatants by the Griess assay, finding a dose-dependent increase by up to 37% at 200 μg/mLof ROFA(control: 3.9 ± 0.3nmol NO2-/mg protein, p<0.01), while no significant differences were observed after CAPs incubation.Moreover, cell culture supernatants from both ROFA- and CAPs-exposed cells showed increased levels of TNF-αand IL-6. Given that ROFA and CAPs differ in elemental composition, PM chemistry might be determinant for the reported effects. These findings suggest that alveolar macrophagesare in part responsible for the oxidative and inflammatory response observed after the exposure to environmental PM, and therefore contribute to the understanding of the cellularpathways triggered by PM inhalation.
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Palabras Clave
MACROPHAGESOXIDATIVE/IMMFLAMATORY RESPONSEPARTICULATE MATTERAIR POLLUTION