Oxidative stress has been implicated in the etiology of many pathological states and known to result in DNA damage. Oxidative DNA damage can lead to mutagenesis (1 –3 ) and has been associated with aging (4 ), diabetes mellitus (5 ), inflammatory disease (1 ) and carcinogenesis (1 –3 ,6 ). The 8-hydroxy-2-deoxyguanosine lesion (8-OHdG) is often used in the assessment of oxidative DNA damage and has become the de facto marker for oxidative damage to DNA. 8-OHdG is one of the most prominent lesions observed following exposure to ionizing radiation (7 ) but also results from treatment with many xenobiotics (8 ) as well as by endogenous mechanisms. Thus, normal endogenous levels becomes a critical issue in the assessment of cellular 8-OHdG levels in pathological states. Furthermore, 8-OHdG is efficiently repaired by a DNA glycosylase specific for this lesion (9 ) and its contribution to mutagenesis is relatively weak (10 –12 ). However, it is representative of approximately 20 additional oxidatively-denved lesions known to result from radiation damage (13 ) and whose mutagenic outcome are largely unknown in mammalian-cell systems.
