Journal
TOXICOLOGY IN VITRO
Volume 51, Issue -, Pages 106-113Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2018.05.007
Keywords
Copper; Papillary muscles; Myocardial contractility; Oxidative stress; Myosin-ATPase
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Funding
- CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior) [23038.006534/2016-93]
- CAPES/PNPD (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - PNPD-Institucional)
- FAPES/CNPq (Fundacao de Amparo a Pesquisa do Espirito Santo/Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) [48511935/2009 PRONEX]
- Edital universal/CNPq [44181/2014-9]
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Copper is an essential metal for homeostasis and the functioning of living organisms. We investigated the effects of a high copper concentration on the myocardial mechanics, investigating the reactive oxygen species (ROS) mediated effects. The developed force of papillary muscles was reduced after acute exposure to a high copper concentration and was prevented by co-incubation with tempol, DMSO and catalase. The reuptake of calcium by the sarcoplasmic reticulum was reduced by copper and restored by tempol. The contractile response to Ca2+ was reduced and reversed by antioxidants. The response to the beta-adrenergic agonist decreased after exposure to copper and was restored by tempol and catalase. In addition, the in situ detection showed increased O-2 - and OH. Contractions dependent on the sarcolemmal Ca2+ influx were impaired by copper and restored by antioxidants. Myosin-ATPase activity decreased significantly after copper exposure. In conclusion, a high copper concentration can acutely impair myocardial excitation-contraction coupling, reduce the capacity to generate force, reduce the Ca2+ inflow and its reuptake, and reduce myosin-ATPase activity, and these effects are mediated by the local production of O-2 -, OH and H2O2. These toxicity effects of copper overload suggest that copper is a risk factor for cardiovascular disease.
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