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MOREIRA, R. P. Contribution of NAD(P)H oxidase complex in dysfunction of the thoracic aorta of young mice treated with cholesterol. 2014.69f. Dissertation. Faculdade de Ciências Farmacêuticas de Ribeirão Preto – Universidade de São Paulo, Ribeirão Preto, 2014. Several factors are responsible for the development of cardiovascular disease, including high cholesterol intake. According to AMH, the recommended intake of cholesterol is 300 mg/ daily, however these values are not always respected. Most often the consequence of high cholesterol consumption is the development of dyslipidemia, which favors the development of endothelial dysfunction. It is described that a high intake of cholesterol can lead to the risk of developing cardiovascular disease even before the development of dyslipidemia, since in some cases the recommended daily intake of cholesterol in the diet is exceeded, and even chronic stages of consumption not observing the development. Thus, chronic exposure to high concentrations of cholesterol could promote changes in the vascular system, even before the installation process dyslipidemic. The aim of this work was to study the effects of ingestion of high concentrations of cholesterol in mice on the responses to angiotensin II (Ang II) in the thoracic aorta, as well as evaluate the involvement of NAD(P)H oxidase in this process. The animals were divided into groups treated with 1% cholesterol diet (CD) or standard chow (SC) for 1 month or 3 months. Treatment with SC did not change the weight of the animals was not observed morphological changes in the thoracic aorta, suggesting that the change in the functionality of this tissue was not due to structural changes. Treatment with SC resulted in increased basal levels of O 2, produced in part by NOX1 and NOX4, in addition to increased protein expression of NOX1 in the thoracic aorta of animals treated three months . In the functional study, we observed an increase in the Emax of Ang II in animals treated for 1 month and 3 months, an independent response of endothelium. This increase was restored in the presence of Tiron, showing the contribution of O 2 in increasing the Emax of Ang II in the thoracic aorta. In the presence of inhibitors of NOX-1 and NOX-4 was also observed Emax restoration observed in the absence thereof, showing the involvement of subunits for the production of O 2. The animals treated with CD showed no changes in lipid profile, this is due largely to the lack of cholic acid in the diet. The Emax of Ang II was increased in the thoracic aorta of mice treated with CD as a result of an increase in basal levels of O 2, produced by NOX1 and NOX4. The basal levels of O 2 increased this should possibly reacting with NO decreasing its availability, thereby increasing the contractile effects of Ang II in thoracic aorta. Some hypotheses were proposed to explain the increased basal O 2 in the thoracic aorta. 1o Increase in the concentration of cholesterol in lipid pockets present in caveolae. 2o Formation of oxysterols; 3o microparticle formation . The results obtained and the hypotheses in this work, as an increase in the production of oxysterols and microparticles can serve as potential targets for the development of studies of new markers, and early diagnosis of vascular alterations caused by excessive consumption of cholesterol began in young individuals.

Contribuição do complexo NAD(P)H oxidase na disfunção de aorta torácica de camundongos jovens tratados com colesterol