During HF ROS production is chronically increased due to the uncoupling of the mitochondrial electron transport chain, the increase in energy demand, the switch from fatty acids to glucose as an energy substrate in cardiomyocytes (Mak and Newton, 2001; Ventura-Clapier et al., 2004), upregulation of nitric oxide synthase (NOS), xanthine oxidase and NADPH oxidase (NOX), and decreased reduced glutathione (Zima and Mazurek, 2016; Nikolaienko et al., 2018). This evidence concerns the gene NOS1 and hydrops fetalis.