From air to heart: Particle pollution (PM2.5) and induced injury on cardioblast cells

Abstract

This study evaluated toxicological effects owing to fine particulate matter (PM2.5) exposure in cardioblast cells (H9c2 lineage). The cells were treated with different particulate matter extract solutions for 24 h, F100% (1g of filter containing PM2.5 per 100 mL culture medium, used as stock), F50% (1/2 F100) and F10% (10% of stock). Cell viability, the production of reactive oxygen species (ROS), antioxidant capacity, lipid damage, necrosis, and apoptosis parameters were measured to assess cell damage. The results showed that cell injuries are related to increasing exposure concentrations. Effects exposure to PM2.5 in F10% was no harmful for H9c2 lineage. The lactate dehydrogenase activity and damage lipid membrane were increased in cells exposed to F50% and F100%. The ROS production was higher and total antioxidant capacity lower in F50% and F100% concentrations. Catalase activity decreased only in the F100% group. Apoptosis and necrosis percentages were higher for F50% and F100% groups. In the PM2.5 extracts some metals were detected (Co, Cd, Li, Mn, Ni, Sr, Ba, Rb, Cu, Pb, As, Zn, Al, Ti, Fe, Si, K, V), which could contribute for toxicological effects in H9c2 lineage. In conclusion, higher concentrations of PM2.5 in solutions were able to elicit cell injury and death cardiac cells in H9c2 through elevation ROS levels, imbalance redox, lysis membrane cell, necrosis and apoptosis.