Damage to DNA by environmental and endogenous agents is considered to be a critical step leading to mutation and subsequent neoplastic transformation and cancer induction. It is also a key event in the cytotoxicity induced by several anti-cancer agents such as ionizing radiation and many of the commonly used chemotherapeutic agents. To counter insult to their DNA by genotoxic agents, cells have recourse to a variety of DNA repair pathways that each deal with a different class of lesions (1 ). Because of the pivotal role played by DNA damage and repair in carcinogenesis and cancer therapy, there is a clear need to be able to detect and quantify the damage. In addition to their use in laboratory studies of the biochemistry and genetics of mutagen-esis and DNA repair, such assays present the possibility of using DNA damage as an endpoint in monitoring environmental and occupational exposure to carcinogens and in clinical dosimetry of cellular exposure to anti-cancer agents.