Avaliação da atividade das ectonucleotidases em resposta aos efeitos adversos causados pela exposição a 2,3,7,8- Tetraclorodibenzeno-p-dioxina (TCDD) utilizando zebrafish (Danio rerio) como modelo de estudo

Detalhes bibliográficos
Ano de defesa: 2011
Autor(a) principal: Azevedo, Mariana Barbieri de
Orientador(a): Bogo, Maurício Reis
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Pontifícia Universidade Católica do Rio Grande do Sul
Porto Alegre
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://hdl.handle.net/10923/1439
Resumo: The 2,3,7,8-tetrachlorodibenzeno-p-dioxin (TCDD) is a member of a group of environmental contaminants known as polychlorinated aromatic hydrocarbon and can be formed during the chlorine bleaching process used by pulp and paper and as a byproduct of the manufacture of certain chemicals. Once associated with ligands such as TCDD, the aryl hydrocarbon receptor (AHR) is translocated into the nucleus where it will form a dimer with nuclear translocator aryl hydrocarbon receptor (ARNT). The heterodimer AHR/ARNT formed, regulates the expression of a number of genes involved in cellular response to environmental changes and development conditions. Among the genes, is the coding for an ecto-ATPase (NTPDase2). Thus, it becomes important to assess the acute exposure (in vivo) of TCDD on the hydrolysis of ectonucleotidases in zebrafish brain membranes. The ectonucleotidases are enzymes capable of hydrolyzing the nucleotides and inactivating the signaling mediated by extracellular nucleotides. Among the ectonucleotidases, there are the NTPDase and ecto-5'-nucleotidase. The NTPDase activity showed no significant difference in the hydrolysis of ATP and ADP, as well as in AMP in menbranes of zebrafish. These findings seem to be important to reinforce the idea that NTPDase2 gene induction cannot be a general pathogenic factor in TCDD toxicity. However, further studies using either higher doses of TCDD and long-term exposure are required.