The study by Ohara, Peterson, and Harrison investigates the increased production of superoxide anion (O2-) in hypercholesterolemic vessels (HV) compared to normal vessels (NV). Using a chemiluminescence assay based on lucigenin, they found that HV produced three times more O2- than NV. Endothelial removal increased O2- production in NV but decreased it in HV. Oxyquinol, a noncompetitive inhibitor of xanthine oxidase, normalized O2- production in HV but had no effect in NV. In isometric tension studies, oxyquinol improved acetylcholine-induced relaxations in HV but not in NV. These findings suggest that the increased O2- production in HV is likely due to xanthine oxidase activation and may contribute to the early atherosclerotic process by inactivating endothelium-derived nitric oxide and generating other oxygen radicals.The study by Ohara, Peterson, and Harrison investigates the increased production of superoxide anion (O2-) in hypercholesterolemic vessels (HV) compared to normal vessels (NV). Using a chemiluminescence assay based on lucigenin, they found that HV produced three times more O2- than NV. Endothelial removal increased O2- production in NV but decreased it in HV. Oxyquinol, a noncompetitive inhibitor of xanthine oxidase, normalized O2- production in HV but had no effect in NV. In isometric tension studies, oxyquinol improved acetylcholine-induced relaxations in HV but not in NV. These findings suggest that the increased O2- production in HV is likely due to xanthine oxidase activation and may contribute to the early atherosclerotic process by inactivating endothelium-derived nitric oxide and generating other oxygen radicals.