Abstract

Since bacterial excision repair was last reviewed not only has the understanding of previously recognized mechanisms increased, but new mechanisms have been described which have broadened the concept of excision repair to include possible roles of glycosylases, insertases, and demethylases. In addition, the importance of interrelations between the inducible and constitutive responses to lesions in DNA has become evident. However, the relationships of biological end points, such as survival and mutagenesis, to the biochemical criteria of responses to DNA damage, remain obscure. This is a particularly serious problem in the case of mammalian cells, since the relevant biological end point may not be known. Survival and mutagenesis of cells in culture are not necessarily directly related to the function of cells in the organism. However, the colony-forming ability of irradiated XP cells does appear to correlate with the severity of the patients neurological symptoms, and the excision-repair capability of cultured human cells may correlate with mutation and survival after exposure to UV and chemical carcinogens. Further analysis of responses to DNA damage may clarify their role in abnormal differentiation and malignant transformation. 404 references.

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