Análise do estresse oxidativo e morte celular por material particulado da queima da Amazônia e compostos isolados

摘要

In recent discussions on environmental issues, air pollution has been considered an important environmental risk factor, and, consequently, a burden to human health. Several poluents are released daily by natural or human activities, causing the air to be improper and harmful to the welfare of humans and ecosystems. In the Amazon region, deforestation and forest fires have been causing damage to the exposed population. Studies already demonstrated that airborne particles can lead to serious cardiorespiratory effects, including DNA damage. Therefore, the aim of this study was to evaluate oxidative stress, mitochondrial integrity and cell death caused by organic chemical compounds from particulate matter smaller than 10 μm (PM10) originated from biomass burning of the Amazon forest, as well as the effects of retene, a biomass burning marker, in human lung epithelial cells (A549). It was evaluated reactive oxygen species (ROS) generation (DCF and MitoSOX) and autophagy process by expression and distribution of LC3 protein, autophagosome marker, in A549 cells exposed to 200 μg/mL and 400 μg/mL for 24 h and 72 h. Likewise, it was examined the effects of retene on oxidative stress on the concentrations of 3,3 ng/mL, 10 ng/mL and 30 ng/mL. Also, mitochondrial function and cell death was observed with TMRM and Mitotracker dyes and annexin and propidium iodide markers, respectifully. Regarding the extracted organic particulate matter, this led to the increased production of reactive oxygen species and intracellular mitochondrial superoxide. Additionally, PM10 exposure triggered the formation of autophagosomes, suggesting increased autophagy. In the biological analysis with retene, the data showed that this compound led to an increase in reactive oxygen species and mitochondrial superoxide, hyperpolarization of the mitochondrial membrane, as well as increased mitochondrial content at all tested times. However, the retene was only able to induce cell death in the greatest concentration used and over a 72-hour period. From these results, it is important to emphasize the reduction of emissions by biomass burning, searching for new control policies. In addition, the toxicity of the retene, a biomass burning marker, raises an alert about the inclusion of this compound in the risk assessment of polycyclic aromatic hydrocarbons (PAHs).