Oxidative DNA damage resulting from reactive oxygen species (ROS) is associated with numerous clinical conditions.  ROS, including the physiologically prevalent hydroxyl radical, are generated by reaction of many transition metal ions with H₂O₂ in Fenton or Fenton-like reactions.  Such reactions are site specific in the presence of DNA, with guanine being oxidized to 8-hydroxy-2'-deoxyguanosine (8-OH-dG), an accepted marker of oxidative DNA damage.  Reactions of Cu (II), Fe (II), and Cr (III) with H₂O₂ were performed in the presence of the nucleoside 2'-deoxyguanosine (dG) and the nucleotide 2'-deoxyguanosine-5'-monophosphate (dGMP).  Overall extent of damage and product distribution appear dependent on metal ion binding with N7 of the guanine base and/or the phosphate group.  Metal-phosphate interactions appear to enhance damage from Cr (III) and have little effect on damage involving Cu (II).  Fe (II)-generated damage appears dependent on a combined interaction with both the base and the phosphate.