Avaliação da deposição de placa aterosclerótica e disfunção vascular em aorta de camundongos ApoE-/- após exposição crônica ao cádmio

Detalhes bibliográficos
Ano de defesa: 2018
Autor(a) principal: Oliveira, Thiago Fernandes de
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal do Espírito Santo
BR
Mestrado em Ciências Fisiológicas
Centro de Ciências da Saúde
UFES
Programa de Pós-Graduação em Ciências Fisiológicas
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
612
Link de acesso: http://repositorio.ufes.br/handle/10/7911
Resumo: Introduction: Cadmium exposure is related to cardiovascular diseases, including hypertension and atherosclerosis, which are linked to oxidative stress induced by this metal. Objective: the present study investigated whether the exposure to cadmium promotes the formation of atherosclerotic plaque and promotes endothelial dysfunction in the aorta, in addition to oxidative stress in knockout mice for lipoprotein E (ApoE-/- ). Methods: Experiments were performed on 14 week-old male C57BL / 6 and ApoE-/- mice treated with cadmium chloride (100 mg / L CdCl2 in drinking water for 28 days) or vehicle (distilled water). After exposure to the metal a cholesterol dosage was made and vascular reactivity in response to phenylephrine, acetylcholine or sodium nitroprusside were analysed in the isolated aorta. Bone marrow cells were isolated to evaluate the production of nitric oxide and reactive species of oxygen and nitrogen and the atherosclerotic plaque in the aortic arch was measured. Result: ApoE-/- mice exposed to cadmium showed higher levels of cholesterol than the animals that were not exposed. Cadmium exposure reduced acetylcholine induced relaxation in ApoE-/- , although it did not alter the responses elicited by phenylephrine or sodium nitroprusside. L-NAME incubation reduced the vasodilator response to acetylcholine, but this effect was smaller in cadmium treated ApoE-/- mice, suggesting a reduction in nitric oxide bioavailability. In addition, in cells hematopoietic, cadmium decreased cytoplasmic levels of nitric oxide and increased superoxide anion, hydrogen peroxide and peroxynitrite in ApoE-/- mice exposed to cadmium. Morphological analysis showed that cadmium-treated ApoE-/- mice exhibited increased plaque deposition in the aorta by approximately 3-fold comparing to the non-treated ApoE-/- mice. Conclusion: our results suggest that a cadmium exposure induces endothelial dysfunction in ApoE-/- mice. In addition, cadmium increased cholesterol plasmatic levels, which may promote the development of atherosclerosis in the aorta of ApoE-/- mice. Our findings support a hypothesis that the exposure to cadmium may increase the risk of atherosclerosis development.