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Abstract
DNA damage plays a major role in mutagenesis, carcinogenesis and ageing. The vast
majority of mutations in human tissues are certainly of endogenous origin. A thorough
knowledge of the types and prevalence of endogenous DNA damage is thus essential for
an understanding of the interactions of endogenous processes with exogenous agents
and the influence of damage of endogenous origin on the induction of cancer and other
diseases. In particular, this seems important in risk evaluation concerning exogenous
agents that also occur endogenously or that, although chemically different from endogenous
ones, generate the same DNA adducts. This knowledge may also be crucial to the development
of rational chemopreventive strategies. A list of endogenous DNA-damaging agents,
processes and DNA adduct levels is presented. For the sake of comparison, DNA adduct
levels are expressed in a standardized way, including the number of adducts per 10(6)
nt. This list comprises numerous reactive oxygen species and products generated as
a consequence (e.g. lipid peroxides), endogenous reactive chemicals (e.g. aldehydes
and S-adenosylmethionine), and chemical DNA instability (e.g. depurination). The respective
roles of endogenous versus exogenous DNA damage in carcinogenesis are discussed.