Also MPO was reported to control eNOS activity and/or nitric oxide bioavailability by direct reaction of the MPO compound 1 (highly oxidized iron intermediate during the reaction cycle of peroxidases) with nitric oxide, thereby consuming the vasodilator (Baldus et al, 2004; Eiserich et al, 2002; Rudolph et al, 2012) and thereby inducing endothelial dysfunction (Abdo et al, 2017; Stocker et al, 2004). Here, MPO is linked to endothelial dysfunction.