Direct and Indirect Effect of Air Particles Exposure Induce Nrf2-Dependent Cardiomyocyte Cellular Response In Vitro.

Area of Science:

• Environmental Health
• Cardiology
• Toxicology

Background:

• Air particulate matter (PM) is linked to cardiorespiratory issues, causing cytotoxic and pro-inflammatory effects.
• PM can impact cardiac tissue directly via translocation or indirectly through systemic inflammation.
• Understanding these mechanisms is crucial for public health, especially in urban environments.

Purpose of the Study:

• To investigate the direct and indirect effects of Urban Air Particles from downtown Buenos Aires (UAP-BA) and residual oil fly ash (ROFA) on cardiomyocytes (HL-1 cells).
• To assess the role of reactive oxygen species (ROS) and Nrf2 expression in mediating these effects.
• To explore the potential involvement of lung-derived mediators in particle-induced cardiac alterations.

Main Methods:

• HL-1 cells were directly exposed to UAP-BA and ROFA.
• Indirect exposure involved conditioned media (CM) from particle-exposed alveolar macrophages (AM).
• Metabolic activity (MTT assay), ROS generation (DHR 123), and Nrf2 expression (immunocytochemistry) were measured.

Main Results:

• Direct exposure to UAP-BA and ROFA increased ROS generation in cardiomyocytes, but metabolic activity was preserved due to increased Nrf2 expression.
• Indirect exposure via CM significantly reduced cardiac metabolic activity, associated with elevated ROS and lack of nuclear Nrf2 translocation.
• These findings suggest distinct responses to direct versus indirect particle exposure.

Conclusions:

• Both direct and indirect exposure to particulate matter affect cardiomyocytes in vitro.
• Direct PM exposure triggers protective Nrf2 responses, while indirect exposure via lung inflammation leads to cardiac dysfunction.
• The study supports the hypothesis that lung-derived mediators play a role in particle-induced cardiac damage.