“…ROS also attack polyunsaturated fatty acid residues of phospholipids, resulting in a decreased membrane fluidity, increased leakiness of the membrane, and inactivation of receptors and ion channels, as well as the formation of lipid peroxides and their by-products malondialdehyde (MDA), 4-hydroxy-2-nonenal (both mutagenic and toxic) and F 2 -isoprostanes ( Figure 1) [1][2][3]. Additionally, ROS and RNS may induce damage to proteins, either reversible (such as the formation of mixed disulfides between protein thiol groups and low-molecular-weight thiols, in particular GSH (S-glutathionylation)) or irreversible (carbonylation, nitrosylation and hydroxylation, resulting in generation of carbonylated proteins, nitrotyrosine, 3,4-dihydroxy-phenylalanine, ortho-tyrosine and meta-tyrosine) [1, 5,6]. Such modifications can be detected in cardiovascular (e.g.…”