Efeitos do estresse oxidativo em células de medula óssea, sangue e aorta de camundongos apoe knockout" por "Aterosclerose e envelhecimento- Efeitos do estresse oxidativo em células de medula óssea, sangue e aorta

• Autor(a) principal: Tonini, Clarisse Loureiro
• Data de Publicação: 2013
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/8053
• topic: Aterosclerose; Camundongo Apoe-ko; Envelhecimento; Estresse oxidativo; Fisiologia; 612

The relationship between production of reactive oxygen species and the development of atherosclerosis has been studied for decades. It is known that all inflammatory processes involved in plaque progression leads to increased production of free radicals. Furthermore, aging is a factor that aggravates atherosclerotic disease and also reactive oxygen species production, probably by the loss of antioxidant capacity that makes regular balancing of reactive oxygen species. The Apolipoprotein E deficient mouse is a model widely used in the study of atherosclerosis, in which there is high hypercholesterolemia that results in increased production of reactive oxygen species in the bone marrow, blood and aorta cells. Aging in turn also leads to increased production of reactive oxygen species, however when combined with hypercholesterolemia, the result of this phenomenon is the occurrence of increased production of reactive oxygen species and thus high levels of oxidative DNA fragmentation and apoptosis. In this regard, most notably is the analysis of bone marrow cells, a source of blood and stem cells for all organism that commonly presents a low oxygen tension ambient, in which we showed high generation of superoxide radicals and hydrogen peroxide. Thus, bone marrow is affected by oxidative imbalance caused by aging and atherosclerosis. Still, corroborating these data, in the analysis of DNA fragmentation by comet assay, bone marrow cells showed high levels of fragmentation in atherosclerotic and aged animals. Still, blood and aorta cells from atherosclerotic and aged animals also showed high superoxide anion production. However, there are low hydrogen peroxide production in endothelial cells of all groups, suggesting a possible modulation of tissue-specific effects of antioxidant enzymes. Furthermore, we note that there is not increased production of hydrogen peroxide in blood cells from aged C57 animals, unlike bone marrow mononuclear cells, in which we observed an increase. Finally, it can be noted that, in general, atherosclerosis increases the production of reactive oxygen species as well as aging, but when these two parameters are combined oxidative stress is further increased. The analysis of scientific literature suggests a possible activation of NADPH oxidase enzyme, responsible for the increased production of reactive oxygen species, and downregulation of antioxidant enzymes, which affect the balance of oxidative stress in tissues.