Submitted by Automa??o e Estat?stica (sst@bczm.ufrn.br) on 2017-03-20T22:52:55Z No. of bitstreams: 1 MilenaSimoesPeixoto_DISSERT.pdf: 3229732 bytes, checksum: 280f7905e8a552967b42f0794a5a52f9 (MD5) / Approved for entry into archive by Arlan Eloi Leite Silva (eloihistoriador@yahoo.com.br) on 2017-03-24T19:20:37Z (GMT) No. of bitstreams: 1 MilenaSimoesPeixoto_DISSERT.pdf: 3229732 bytes, checksum: 280f7905e8a552967b42f0794a5a52f9 (MD5) / Made available in DSpace on 2017-03-24T19:20:37Z (GMT). No. of bitstreams: 1 MilenaSimoesPeixoto_DISSERT.pdf: 3229732 bytes, checksum: 280f7905e8a552967b42f0794a5a52f9 (MD5) Previous issue date: 2016-09-19 / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico (CNPq) / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior (CAPES) / A polui??o atmosf?rica ? um fator de risco ambiental, e consequentemente, um problema a sa?de. Diversas subst?ncias s?o lan?adas diariamente por meio de atividades antropog?nicas ou naturais, tornando o ar impr?prio e nocivo ao bem-estar de seres humanos e prejudicial ? fauna e ? flora. Na regi?o amaz?nica, os desmatamentos e as queimadas t?m causado preju?zos para a popula??o exposta. Estudos demonstram que essas part?culas presentes no ar causam s?rios problemas respirat?rios e cardiovasculares, incluindo danos ao DNA. Diante disso, o objetivo desse estudo foi avaliar o estresse oxidativo, a integridade mitocondrial e morte celular desencadeados por compostos org?nicos do material particulado menor que 10 ?m (MP10) oriundos da queima de biomassa da floresta Amaz?nica, assim como os efeitos do reteno, marcador de queima de biomassa, em c?lulas epiteliais do pulm?o humano (A549). Para tal, foi avaliado a forma??o de esp?cies reativas de oxig?nio (ERO) com os corantes DCF e MitoSOX e o processo de autofagia por express?o e distribui??o das isoformas da prote?na LC3, marcadora de autofagossomo maduro, em c?lulas A549 expostas a 200 ?g/mL e 400 ?g/mL de MP10 nos tempos de 24 h e 72 h. Da mesma forma, foi analisado os efeitos do reteno sobre estresse oxidativo nas concentra??es de 3,3 ng/mL, 10 ng/mL e 30 ng/mL. Tamb?m foi observado a fun??o mitocondrial com TMRM e Mitotracker e o processo de morte celular via marca??o por anexina e iodeto de prop?deo. Com rela??o ? fra??o org?nica do material particulado, esta induziu um aumento da produ??o de ERO intracelulares e de super?xido mitoncondrial. Al?m disso, a exposi??o ao MP10 desencadeou a forma??o de autofagossomos, sugerindo o aumento da autofagia. Nas an?lises biol?gicas com o reteno, os dados mostraram que este composto levou ao aumento de ERO e de super?xido mitocondrial, a hiperpolariza??o da membrana mitocondrial, assim como o aumento do conte?do mitocondrial em todos os tempos testodos. Por?m, o reteno s? foi capaz de induzir a morte celular na maior concentra??o utilizada e no per?odo de 72 h. Com esses resultados, ? importante enfatizar a necessidade de redu??o da emiss?o de poluentes por queima de biomassa, buscando pol?ticas de controle. Al?m disso, a toxicidade apresentada pelo reteno levanta um alerta em rela??o a inclus?o desse composto, marcador de queima de biomassa, na avalia??o de risco dos hidrocarbonetos polic?clicos arom?ticos (HPA). / 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 ?m (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 ?g/mL and 400 ?g/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).