ABC | Volume 114, Nº2, February 2020

Original Article Stefani et al. DNA damage and heart failure Arq Bras Cardiol. 2020; 114(2):234-242 Figure 1 – Image of cells submitted to SCGE (comet assay) of left ventricle, lungs, diaphragm, gastrocnemius and soleus of Sham-operated and rats with CHF. Panel A: Isolated cells of the respective tissue of Sham-operated rat. Panel B: Isolated cells of the respective tissue of rat with MI-induced CHF. Slides stained with silver nitrate. The image shows no formation of comets in Panel A, but in Panel B the image shows the formation of comets with distinct tails. The length of the tail represents the single strand and double strand breaks of nuclear DNA (magnification of 20x, scale bar of 20 µm). Sham-operated Chronic Heart Failure Sham-operated Left Ventricle Lungs Diaphragm Gastrocnemius Soleus Chronic Heart Failure Sham-operated Chronic Heart Failure Sham-operated Chronic Heart Failure Sham-operated Chronic Heart Failure concentrations of 8-OHdG in CHF patients. 28 The rationale for higher concentrations of DNA oxidative products indicates that the higher extent of genotoxic damage is highly contributed to the oxidation of mitochondrial DNA. 29 Cardiac myocytes present the highest content of mitochondria, which could indicate higher formation of ROS and contribute significantly to mitochondrial dysfunction. This study did not quantify the concentration of 8-OHdG, however we considered DNA damage that is widely used in order to evaluate DNA strand breaks. The study by Jaenisch et al., 30 also developed by our 238