Nanoparticles in Medicine: A Focus on Vascular Oxidative Stress

Figure 5

Effects of nanoparticles on the main mechanisms of vascular oxidative stress and antioxidant systems. Mitochondrial respiratory chain enzymes, xanthine oxidase (XO), NADPH oxidase (Nox), and uncoupled endothelial NO synthase (eNOS) are the main sources of superoxide anion (O₂⁻) in the vascular wall. O₂⁻ can produce hydroxil radical (OH), hydrogen peroxide (H₂O₂), and peroxynitrite (ONOO⁻). The enzymes that decompose H₂O₂ are catalase, glutathione, thioredoxin peroxidase, and peroxiredoxin. In inflammation, the induction of iNOS produces high levels of NO which react with mitochondrial respiratory chain enzymes and increase O₂⁻ production. Some nanoparticles (NPs), such as nanoceria, have demonstrated the ability to reduce the expression of iNOS. Moreover, nanoceria can scavenge both NO and OH, thus proving to be anti-inflammatory and antioxidant agents. Some NPs increase Nox activity and can be used as antitumoral agents. The role of Nox 4 in vascular function is controversial; whereas some studies report a protective role against atherogenesis, others show the contrary. Certain NPs can be used as NO donors to reverse endothelial dysfunction. Some NPs exert SOD, catalase, oxidase, phosphatase, and peroxidase-mimetic activities.