Producción CyT
Congreso
Autoría
Marchini T
;
Garcés M
;
Calabró V
;
PAZ, MARIELA LAURA
;
Lago N
;
Cáceres L
;
Vico T
;
Guaglianone A
;
Vanasco V
;
González Maglio DH
;
Berra A
;
Alvarez S
;
Evelson PA
Fecha
2017
Editorial y Lugar de Edición
Fundación Revista Medicina
Resumen
Información suministrada por el agente en
SIGEVA
The exposure to air pollution leads to increased morbidity and mortality rates from cardiorespiratory diseases. In has been suggested that local and systemic oxidative stress and inflammation play a central role in this scenario. The aim of this work was to characterize a mice model of continuous exposure to urban air pollution, by the assessment of different markers of pulmonary, systemic, and cardiac oxygen metabolism and inflammation. 8-week-old balb/c male mice were exposed to urban or filt...
The exposure to air pollution leads to increased morbidity and mortality rates from cardiorespiratory diseases. In has been suggested that local and systemic oxidative stress and inflammation play a central role in this scenario. The aim of this work was to characterize a mice model of continuous exposure to urban air pollution, by the assessment of different markers of pulmonary, systemic, and cardiac oxygen metabolism and inflammation. 8-week-old balb/c male mice were exposed to urban or filtered air (control) inside a chamber located in a highly populated area of Buenos Aires City. Animals were exposed for 8 h/day, 5 days/week, for up to 3 months. After 2 months, mice exposed to urban air pollution showed a 53% increase in total leucocytes in bronchoalveolar lavage (BAL) samples in comparison with the control group (control: 1.0±0.2 x105 cells, p<0.001), together with a 104% increase in BAL protein concentration (control: 0.15±0.03 mg/mL, p<0.05). Both BAL leucocytes and protein concentration were still significantly increased after 3 months in exposed mice in comparison with the control group. NADPH oxidase activity was increased in lung homogenates by 25% (control: 1.33±0.03 AU/mg protein, p<0.05) after 2 months. While no differences were observed in total lung oxygen consumption at any evaluated time point, cardiac oxygen consumption decreased by 37% in exposed mice in comparison with the control group after 2 months (control: 980±50 nmol O2/min g tissue, p<0.05), and by 32% after 3 months (control: 1100±90 nmol O2/min g tissue, p<0.01). A slight, yet not significant increase was observed in plasma TNF-α and IL-6 levels in exposed mice. The present data suggest that a continuous exposure to urban air leads to lung inflammation and decreased cardiac oxygen metabolism, which may explain some of the adverse health effects associated with the exposure to air pollution.
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Palabras Clave
MICEOXIDATIVE STRESSINFLAMMATIONAIR POLLUTION