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In vitro testing of estrogen agonists for the evaluation of reactive oxygen species production in glioma cells

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Resumo:Compelling evidence show that cell exposures to 17β-estradiol (E2) trigger intracellular reactive oxygen species (ROS) production. These species play an important role in both tumor development and responses to anticancer strategies and their accumulation in normal cells leads to the occurrence of numerous oxidative reactions which can cause overwhelming damages and promote cell apoptosis. Nevertheless, there is an elevated basal level of oxidative stress in cancer cells, which is balanced by their increased antioxidative capacity. This fact suggests cancer cells may be more susceptible to further oxidative stress than normal cells and strategies that explore these pathways would increase the lethality of anticancer agents. In this study, exposures of cancer cells to estrogen agonists are made and fluorescence techniques used in the attempt to lead cells to apoptosis by increasing their oxidative stress levels. These exposures are made using 13 estrogen previously-synthetized analogues and four different time points (1h, 2h, 6h and 24h). In the end, the results show that the tested compounds induce a rapid production of ROS but this is not a lasting effect and doesn’t affect cell viability. E2 is the compound with the highest and more stable levels of oxidative stress production.
Autores principais:Tavares, Ana Filipa Pereira
Assunto:Reactive oxygen species (ROS) Anticancer strategies Cell apoptosis Oxidative stress Estrogen agonists Fluorescence techniques Mestrado Integrado - 2014
Ano:2014
País:Portugal
Tipo de documento:dissertação de mestrado
Tipo de acesso:acesso restrito
Instituição associada:Universidade de Lisboa
Idioma:inglês
Origem:Repositório da Universidade de Lisboa
Descrição
Resumo:Compelling evidence show that cell exposures to 17β-estradiol (E2) trigger intracellular reactive oxygen species (ROS) production. These species play an important role in both tumor development and responses to anticancer strategies and their accumulation in normal cells leads to the occurrence of numerous oxidative reactions which can cause overwhelming damages and promote cell apoptosis. Nevertheless, there is an elevated basal level of oxidative stress in cancer cells, which is balanced by their increased antioxidative capacity. This fact suggests cancer cells may be more susceptible to further oxidative stress than normal cells and strategies that explore these pathways would increase the lethality of anticancer agents. In this study, exposures of cancer cells to estrogen agonists are made and fluorescence techniques used in the attempt to lead cells to apoptosis by increasing their oxidative stress levels. These exposures are made using 13 estrogen previously-synthetized analogues and four different time points (1h, 2h, 6h and 24h). In the end, the results show that the tested compounds induce a rapid production of ROS but this is not a lasting effect and doesn’t affect cell viability. E2 is the compound with the highest and more stable levels of oxidative stress production.