Airborne particulate matter exposure impairs lung redox metabolism involved in tissue damage repair mechanisms

MARCHINI T; FREIRE A; MAGNANI N; GARCÉS M; CALABRÓ V; REYNOSO S; CÁCERES L; EVELSON P

Siena

Congreso; The Future of Redox Biology. Siena 2022; 2022

SFRR-I

Airborne pollutants such as particulate matter (PM) are associated with enhanced health risk as they can trigger or aggravate several pulmonary diseases through impairment of the lung redox metabolism and inflammation. Our aim was to assess if lung oxidative metabolism alterations initiated by PM inhalation were associated with a delayed epithelial injury repair. Mice were exposed to filtered air (FA) or urban air (UA) from Buenos Aires City, in whole-body exposure chambers for 8 weeks followed by an epithelial damage induced by intratracheal instillation of 0.1 N hydrochloric acid (HCl). The oxidative metabolism was evaluated 5 days after injury. Breathing UA impairs the redox metabolism modulation involved in lung damage as tissue oxygen uptake was lower in mice exposed to UA compared to the FA group. Moreover, SOD activity showed the same trend, even after the significant increase observed in the transcription factor Nrf2 expression induced by the injury after UA exposure. The increased total cell count and protein concentration found in the bronchoalveolar lavage (BAL) from mice breathing UA may be related to a remain alveolar epithelial disruption. UA-induced alterations in redox regulation may be associated to delayed tissue repair, leading to increased alveolar epithelium permeability and impaired lung function.