Advanced atherosclerotic plaques demonstrate extensive DNA damage, seen in smooth muscle cells, endothelial cells, macrophages and in circulating cells, and in both nuclei and mitochondria.$1$ DNA damage includes both single- or double-stranded breaks, deleted sections of DNA, nucleotide modifications, and extrusions of DNA from the nucleus (micronuclei). Reactive oxygen species (ROS) induce a variety of DNA damage, including oxidatively modified bases, apurinic/apyrimidinic sites, and strand breaks. Guanine is the most readily oxidized base, reacting with $•$OH to generate a reducing neutral radical that reacts with O$2$, and via electron transfer, forms 8-oxo-7,8-dihydroguanine (8-oxo-G).$2$ 8-oxo-G and its products are the most abundant DNA lesions on oxidative exposure, with 1 to 2/10$6$ residues in nuclear DNA and 1 to 3/10$5$ residues in mitochondrial DNA (mtDNA), and up to 10$5$ 8-oxo-G lesions are formed in the cell daily.$1$ Advanced plaques are characterized by extensive accumulation of 8-oxo-G, seen in both macrophages and smooth muscle cells.$\mathrm{<mrow\; data-mjx-texclass="ORD">3,4</mrow>}$ 8-oxo-G is primarily repaired by base excision repair by several enzymes, including specific 8-oxo-G DNA glycosylases I$5$ and II$6$ (OGG1/2) and the Nei-like (NEIL) glycosylases; the excised DNA is repaired by AP endonucleases before gap filling by polymerases and ligation.