Figure 1.

Reactive oxygen species–producing systems in atherosclerosis. MIT oxidative, Mitochondrial oxidative; eNOS, endothelial nitric oxide synthase; ${\text{O}}_2^{•-}$, superoxide; OX, xanthine oxidase; NO^•, nitric oxide; HOCl, hypochlorite; H₂O₂, hydrogen peroxide; ONOO⁻, peroxynitrite; ^•OH, hydroxyl radicals; SOD, enzyme superoxide dismutase; GSH, glutathione; Trx, thioredoxin. ${\text{O}}_2^{•-}$ can be generated in the blood vessel wall by NOXs, uncoupled eNOS, OX, and mitochondrial respiration chains. H₂O₂ can traverse spontaneous transformation to ^•OH by Fe reaction, SOD. H₂O₂ can be detoxified through GSH peroxidase, Trx peroxidase, and catalase to H₂O and O₂. Meanwhile, the myeloperoxidase enzyme can employ H₂O₂ to oxygenize chloride to the strong oxidizer HOCl. The uncoupling eNOS decreases endothelial NO production, which is further aggravated by reduced eNOS expression and activity.