A exposição aguda a alta concentração de cobre prejudica a contratilidade miocárdica: participação das espécies reativas de oxigênio

• Ano de defesa: 2018
• Autor(a) principal: Filetti, Filipe Martinuzo
• 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
• Palavras-chave em Português: Copper; Papillary muscles; Myocardial contractility; Oxidative stress; Myosin-ATPase; Músculos papilares; Contratilidade miocárdica; Estresse oxidativo; ATPase miosínica; Cobre; Coração - Contração; Stress oxidativo; Fisiologia; 612
• Link de acesso: http://repositorio.ufes.br/handle/10/7910

Copper is an essential metal for homeostasis and the functioning of living organisms, but in overload can lead to systemic harmful effects. Copper toxicity can be related to reactive oxygen species (ROS) production and cardiovascular diseases. We testing the effects of high copper concentration (10 μg/mL) on the myocardial mechanics, investigating the ROS-mediated effects. The developed force of papillary muscles was reduced after acute exposure to high copper and prevented by co-incubation with tempol, DMSO and catalase. The indirect evaluation of sarcoplasmic reticulum activity was reduced by copper and restored by tempol. The contractile response to calcium was reduced by copper and reversed by antioxidants. The response to β-adrenergic agonist decreased after exposure to copper and restored by tempol and catalase. Contractions dependent on the sarcolemmal calcium influx were impaired by copper and restored by antioxidants. In addition, in situ detection in papillary muscles showed increased O2 •- and OH• . The myosin-ATPase activity decreased significantly. In conclusion, high copper concentration can acutely impair myocardial excitationcontraction coupling reducing the capacity to generate force, by reducing calcium inflow and of its reuptake, myosin-ATPase activity, and these effects are mediate by local production of O2 •- , OH• and H2O2. These toxicity effects suggest that exposure to high copper concentration is a risk factor for cardiovascular disease