Revisiting the rodent repairadox

Cultured rodent and human cells typically display similar clonal survival c haracteristics following exposure to ultraviolet light (UV). However, compa red to human cells, cultured cells from mice, rats, and hamsters are genera lly deficient in excision repair of the most prominent DNA lesion produced by UV, the cyclobutane pyrimidine dimer. In light of recent studies on the control of nucleotide excision repair, we are beginning to understand the b asis for this so-called "repairadox." The resolution of this issue is impor tant because rodents are so widely employed as surrogates for humans in gen etic toxicology. This article will review the evolution in our understandin g of rodent DNA repair and will also "revisit" my early association with my graduate mentor and esteemed colleague, Dick Setlow, in his honor upon the attainment of his 80th birthday. Environ. Mol. Mutagen. (C) 2001 Wiley-Lis s, Inc.