Name: FILIPE MARTINUZO FILETTI
Publication date: 13/04/2018
Advisor:
Name |
Role |
|---|---|
| DALTON VALENTIM VASSALLO | Co-advisor * |
| MAYLLA RONACHER SIMÕES | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| DALTON VALENTIM VASSALLO | Co advisor * |
| LEONARDO DOS SANTOS | Internal Examiner * |
| MAYLLA RONACHER SIMÕES | Advisor * |
| MIRIAN FIORESI | External Examiner * |
Summary: Copper is an essential metal for homeostasis and the functioning of living organisms. Copper toxicity can be related to reactive oxygen species (ROS) production and cardiovascular diseases. We investigated the effects of high copper concentration 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 reuptake of calcium by sarcoplasmatic reticulum was reduced by copper and restored by Tempol. The contractile response to calcium was reduced and reversed by antioxidants. The response to β-adrenergic agonist decreased after exposure to copper and restored by Tempol and Catalase. In addition, in situ detection showed increased O2- and OH. Contractions dependent on the sarcolemmal calcium influx were impaired by copper and restored by antioxidants. The myosin-ATPase activity decreased significantly. In conclusion, high copper concentration can acutely impair myocardial excitation-contraction coupling reducing the capacity to generate force, the reduction in the calcium inflow and of its reuptake, reduction of myosin-ATPase activity, and these effects are mediate by local production of O2-, OH and H2O2. These toxicity effects of copper overload suggest that copper is a risk factor for cardiovascular disease.
