O estudo ultraestrutural de doenças metabólicas

• Ano de defesa: 2019
• Autor(a) principal: Resgala, Ludmilla Carvalho Rangel
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; BR; Doutorado em Biotecnologia; Centro de Ciências da Saúde; UFES; Programa de Pós-Graduação em Biotecnologia
• Palavras-chave em Português: Osteoporosis; Alzheimer's disease; Amyloidosis; Apolipoprotein E; Tributyltin; Osteoporose; Doenças de Alzheimer; Amiloidose; Apolipoproteína-E; Tributilestanho; Biotecnologia; 61
• Link de acesso: http://repositorio.ufes.br/handle/10/10953

Cell damage can be caused by factors related to aging or caused by stressors. In this study, our general objective was to study the ultrastructure of metabolic diseases. Among the metabolic diseases related to aging, osteoporosis and Alzheimer's disease (AD) are highlighted, and for this study we used C57 Black 6, 12 months old, SHAM, ovariectomized (OVX), APOEKO and APEKO/OVX mice as osteoporosis and AD models. Through ultrastructural analysis, we revealed that damage to the brain of APOEKO animals, such as atherosclerosis, breakdown of the blood-brain barrier, microglial activation, NFT's formation, neuropil loss, were potentiated by estrogen depletion. Our data on bone ultrastructure revealed that damage to the bone microarray of the APOEKO / OVX animals was more severe, as occurred in the brain, when compared to the other groups. In addition, we have described for the first time that amyloidosis in APOEKO animals is potentiated by estrogen deficiency (OVX). Regarding the ultrastructural study of metabolic disease caused by stress, we used as a model Wistar rats treated with 100 ng / kg / day of tributyltin (TBT), a pollutant organotin considered to be highly toxic for 15 days. Our results revealed that TBT stress was able to trigger damage in the bone microarchitecture of the vertebrae of the rats, in a process similar to osteoporosis. In addition, we have seen that bone mineral density (BMD) was lower in the treated rats. Our also demonstrate, for the first time, that TBT is a pollutant capable of promoting serious damage to bone metabolism, such as the development of osteoporosis. Possibly TBT affects the estrogen metabolism in the maintenance of the bone microarchitecture or even erroneously replacing other divalent ions such as Ca2+ or Mg2+ in the formation of the bone mineral matrix.