DNA oxidation has evolved from an exploratory phase to a complex field with significant implications for health and disease. Early research on radiation-induced DNA damage revealed the role of oxygen radicals in causing oxidative lesions, leading to increased interest in DNA oxidation as a source of cancer and other diseases. Various techniques have been developed to measure oxidative DNA damage, including GC-MS and HPLC-EC, which have shown discrepancies due to potential artifactual oxidation. Recent studies have refined these methods, reducing estimates of oxidative DNA damage and improving accuracy. Oxidative DNA adducts, such as oxo $ ^{8} $ dG, are particularly relevant, with their levels showing significant variation depending on the method used. Artifactual oxidation remains a challenge, but recent advancements have improved the reliability of measurements. Oxidative DNA damage occurs through various mechanisms, including the Fenton reaction involving superoxide radicals, iron, and hydrogen peroxide. Other reactive species, such as peroxynitrite, also contribute to DNA oxidation. The damage can be repaired by specific enzymes, such as endonuclease III and Fapy glycosylase, which recognize and remove oxidized bases. These repair mechanisms are conserved across species, with homologs in humans and other organisms. Oxidative damage is also linked to cancer, with evidence showing that factors like smoking, chronic inflammation, and mitochondrial leakage contribute to DNA oxidation and cancer development. DNA oxidation is also associated with aging and developmental abnormalities. Oxidative damage increases with age, particularly in mitochondria, and is linked to various diseases. The repair of oxidative DNA damage is crucial for maintaining genomic stability, and deficiencies in repair mechanisms can lead to increased mutation rates and cancer risk. Recent studies have shown that oxidative damage can be measured in urine and interstitial fluid, providing non-invasive methods for assessing DNA damage. Additionally, techniques like single-cell gel electrophoresis and immunohistochemistry allow for the detection of DNA damage in fixed cells and tissues. The role of oxidative DNA damage in cancer and aging is well established, with evidence showing that oxidative stress contributes to the development of various cancers. The use of transgenic mouse models has provided insights into the mechanisms of oxidative mutagenesis and the effects of oxidative damage on DNA repair. Overall, the study of DNA oxidation continues to reveal important insights into the causes and consequences of DNA damage, highlighting the need for further research to understand and mitigate its effects.DNA oxidation has evolved from an exploratory phase to a complex field with significant implications for health and disease. Early research on radiation-induced DNA damage revealed the role of oxygen radicals in causing oxidative lesions, leading to increased interest in DNA oxidation as a source of cancer and other diseases. Various techniques have been developed to measure oxidative DNA damage, including GC-MS and HPLC-EC, which have shown discrepancies due to potential artifactual oxidation. Recent studies have refined these methods, reducing estimates of oxidative DNA damage and improving accuracy. Oxidative DNA adducts, such as oxo $ ^{8} $ dG, are particularly relevant, with their levels showing significant variation depending on the method used. Artifactual oxidation remains a challenge, but recent advancements have improved the reliability of measurements. Oxidative DNA damage occurs through various mechanisms, including the Fenton reaction involving superoxide radicals, iron, and hydrogen peroxide. Other reactive species, such as peroxynitrite, also contribute to DNA oxidation. The damage can be repaired by specific enzymes, such as endonuclease III and Fapy glycosylase, which recognize and remove oxidized bases. These repair mechanisms are conserved across species, with homologs in humans and other organisms. Oxidative damage is also linked to cancer, with evidence showing that factors like smoking, chronic inflammation, and mitochondrial leakage contribute to DNA oxidation and cancer development. DNA oxidation is also associated with aging and developmental abnormalities. Oxidative damage increases with age, particularly in mitochondria, and is linked to various diseases. The repair of oxidative DNA damage is crucial for maintaining genomic stability, and deficiencies in repair mechanisms can lead to increased mutation rates and cancer risk. Recent studies have shown that oxidative damage can be measured in urine and interstitial fluid, providing non-invasive methods for assessing DNA damage. Additionally, techniques like single-cell gel electrophoresis and immunohistochemistry allow for the detection of DNA damage in fixed cells and tissues. The role of oxidative DNA damage in cancer and aging is well established, with evidence showing that oxidative stress contributes to the development of various cancers. The use of transgenic mouse models has provided insights into the mechanisms of oxidative mutagenesis and the effects of oxidative damage on DNA repair. Overall, the study of DNA oxidation continues to reveal important insights into the causes and consequences of DNA damage, highlighting the need for further research to understand and mitigate its effects.