Protectors or Traitors: The Roles of PON2 and PON3 in Atherosclerosis and Cancer

Figure 2

Schematic presentation of the suggested antioxidative mechanism of PON2 and PON3. A current model for the role of PON2/3 in the development of atherosclerosis. Ubisemiquinone is released from ETC in the mitochondria during Q cycle. Right. In the absence of PON2/3, ubisemiquinone donates electron to molecular oxygen to form superoxide; superoxide generates other reactive oxygen/nitrogen species (RONS), which oxidize LDL to form oxLDL; macrophages engulf oxLDL to form foam cells; foam cells attach to the arterial wall and subsequently develop into atherosclerotic lesions. Left. In the presence of PON2/3 (in wild type mice), ubisemiquinone binds to PON2/3. The binding of PON2/3 and ubisemiquinone prevents superoxide generation thereby preventing the development of atherosclerosis. Note: it is currently unknown if PON2/3 face the matrix side of the inner mitochondrial membrane or the one directed towards the innermembrane space; also, the stoichiometry of PON2/3 versus Q10 is unknown. Abbreviations: I-NADH: ubiquinone oxidoreductase, II: succinate coenzyme Q reductase, III: ubiquinol cytochrome coxidoreductase, IV: cytochrome c oxidase, V-ATP synthase, Cyto c cytochrome c, Q10-coenzyme Q10.