The article by Halliwell and Aruoma reviews the mechanisms and measurement of DNA damage caused by oxygen-derived species in mammalian systems. When cells are exposed to oxidative stress, DNA damage often occurs, primarily through the activation of nucleases and direct reactions of hydroxyl radicals with DNA. Several oxygen-derived species, such as superoxide radical (O2•−), hydrogen peroxide (H2O2), and hypochlorous acid (HOCl), can attack DNA, producing distinct chemical modifications. These modifications, including single-strand breaks, double-strand breaks, and chromosomal aberrations, are measured to assess the extent of oxidative damage and to investigate the mechanisms of DNA damage by ionizing radiation and chemical carcinogens. The authors discuss two main mechanisms of DNA damage induced by oxidative stress: the formation of hydroxyl radicals (•OH) and the activation of nuclease enzymes. •OH can be generated from H2O2 by reaction with metal ions like iron and copper, while nuclease activation is often linked to increases in intracellular calcium ions (Ca2+). Both mechanisms can occur simultaneously, and their relative importance depends on the cell type and the method of oxidative stress induction. The article also explores the mutagenic and carcinogenic effects of reactive oxygen species (ROS). Oxidative stress has been shown to induce mutations in bacteria and mammalian cells, and •OH is classified as a complete carcinogen due to its ability to cause base-pair changes and frameshifts. The relationship between DNA damage and cancer development is complex, involving multiple stages of cellular transformation and the activation of proto-oncogenes. The characterization of chemical changes in DNA by ROS is detailed, including the formation of 8-hydroxyguanine (8-OH-Gua) and thymine glycol, which can lead to mutations and lethality if not repaired. The article highlights the importance of repair systems in removing oxidative lesions from DNA, and the use of urinary excretion of modified bases as a biomarker for oxidative DNA damage. Finally, the authors discuss the measurement of base-derived products as a probe for the mechanism and extent of DNA damage. Techniques such as HPLC coupled with electrochemical detection and gas chromatography/mass spectrometry (GC/MS) are used to identify and quantify the products of DNA damage, providing insights into the role of ROS in DNA damage and their contribution to carcinogenesis.The article by Halliwell and Aruoma reviews the mechanisms and measurement of DNA damage caused by oxygen-derived species in mammalian systems. When cells are exposed to oxidative stress, DNA damage often occurs, primarily through the activation of nucleases and direct reactions of hydroxyl radicals with DNA. Several oxygen-derived species, such as superoxide radical (O2•−), hydrogen peroxide (H2O2), and hypochlorous acid (HOCl), can attack DNA, producing distinct chemical modifications. These modifications, including single-strand breaks, double-strand breaks, and chromosomal aberrations, are measured to assess the extent of oxidative damage and to investigate the mechanisms of DNA damage by ionizing radiation and chemical carcinogens. The authors discuss two main mechanisms of DNA damage induced by oxidative stress: the formation of hydroxyl radicals (•OH) and the activation of nuclease enzymes. •OH can be generated from H2O2 by reaction with metal ions like iron and copper, while nuclease activation is often linked to increases in intracellular calcium ions (Ca2+). Both mechanisms can occur simultaneously, and their relative importance depends on the cell type and the method of oxidative stress induction. The article also explores the mutagenic and carcinogenic effects of reactive oxygen species (ROS). Oxidative stress has been shown to induce mutations in bacteria and mammalian cells, and •OH is classified as a complete carcinogen due to its ability to cause base-pair changes and frameshifts. The relationship between DNA damage and cancer development is complex, involving multiple stages of cellular transformation and the activation of proto-oncogenes. The characterization of chemical changes in DNA by ROS is detailed, including the formation of 8-hydroxyguanine (8-OH-Gua) and thymine glycol, which can lead to mutations and lethality if not repaired. The article highlights the importance of repair systems in removing oxidative lesions from DNA, and the use of urinary excretion of modified bases as a biomarker for oxidative DNA damage. Finally, the authors discuss the measurement of base-derived products as a probe for the mechanism and extent of DNA damage. Techniques such as HPLC coupled with electrochemical detection and gas chromatography/mass spectrometry (GC/MS) are used to identify and quantify the products of DNA damage, providing insights into the role of ROS in DNA damage and their contribution to carcinogenesis.