IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Air pollution particulate matter exposure aggravates myocardial infarction: The role of lung redox metabolism, inflammation and impaired cardiac mitochondrial function
Autor/es:
MARCHINI, TIMOTEO
Lugar:
Evento Virtual
Reunión:
Congreso; SCHCF + ALACF 2020 joint meeting; 2020
Institución organizadora:
Asociación Latinoamericana de Ciencias Fisiológicas (ALACF) y Sociedad Chilena de Ciencias Fisiológicas (SCHCF)
Resumen:
Introduction: Air pollution accounts for 2.4 million deaths from myocardialinfarction (MI) every year. Fine particulate matter (PM2.5) ?airborne particles < 2.5 µm in diameter that mainly arises from dieselexhaust in urban areas ? has been pointed out as the main responsible. However,the underlying mechanisms are not completely understood.Aim: To evaluate the cardiorespiratory and systemic oxidative andinflammatory pathways triggered by PM2.5 inhalation in a combinedmodel of continuous exposure to urban polluted air and experimental MI.Methods: BALB/c mice were exposed to filtered air (FA) or urban air (UA) insidewhole-body inhalation chambers located in Buenos Aires City downtown (12 to 37µg PM2.5/m3) during 16 weeks.Results: After 8 weeks, mice breathing UA showed a 56% increase in total leucocytesin bronchoalveolar lavage (BAL) samples (FA: 1.0±0.2 x105 cells, p<0.05) and a 104% increase in BALprotein concentration (FA: 0.30±0.04 mg/mL, p<0.05).Both were still increased after 12 weeks in UA-exposed mice, together with a3-fold rise in MCP-1 levels. Lung leukocyte recruitment was confirmed byhistology. Oxidative stress might precede inflammation, as increased pulmonaryGSSG and decreased SOD activity, together with increased phospholipidoxidation, were found after 4 weeks. BAL analysis by flow cytometry showedalveolar macrophage accumulation and NO production in UA-exposed mice after 12weeks. In this group, a significantly increased TNF-α and IL-6 plasma levelswere also observed. At this time point, UA exposure induced a 53% increase inischemia/reperfusion injury (FA: 43±4% risk area, p<0.01). Mechanistically, UA exposure lead to impaired cardiacmitochondrial function by decreased active respiration, inner membranedepolarization, increased H2O2 release, and decreased ATPproduction. Conclusion: Air pollution exposure induces a lung response that impairs cardiacmitochondrial function and worsens MI outcome. Our results highlight theimportance of considering environmental factors in the development ofcardiovascular diseases.