AIRBORNE PARTICULATE MATTER EXPOSURE IMPAIRS LUNG REDOX METABOLISM INVOLVED IN TISSUE DAMAGE REPAIR MECHANISMS

REYNOSO SOFIA; MARCHINI TIMOTEO; MARIANA GARCES; CACERES LOURDES; FREIRE AGUSTINA; CALABRÓ VALERIA; BERRA ALEJANDRO; EVELSON PABLO; MAGNANI NATALIA

Congreso; V International Congress in Translational Medicine; 2021

Is estimated that 91% of the world's population breathes polluted air leading to more than 7 million premature deaths per year. Airborne pollutants such as particulate matter (PM) are associated with enhanced health risk as they can trigger or aggravate several pulmonary diseases. Our aim was to assess if alterations in the lung oxidative metabolism initiated by toxicological mechanisms triggered after PM inhalation were associated with a delayed tissue injury repair. To characterize our model, BALB/c mice were exposed to filtered air (FA) or urban air (UA) from Buenos Aires City, in whole-body exposure chambers. Results showed that after 8 weeks of UA exposure, mice developed lung redox alterations and local inflammation without histological damage, therefore that was the time point selected to further evaluate the oxidative metabolism after a moderate lung injury induced by intratracheal instillation of 0.1 N hydrochloric acid (HCl). Pulmonary tissue was evaluated 5 days after HCl treatment. Tissue oxygen consumption was assessed as a whole lung metabolism marker, and the increase observed in mice breathing FA by HCl treatment, was not detected in HCl-mice exposed to UA (p