Revisiting the rodent repairadox.

Abstract:

:Cultured rodent and human cells typically display similar clonal survival characteristics following exposure to ultraviolet light (UV). However, compared to human cells, cultured cells from mice, rats, and hamsters are generally 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 basis for this so-called "repairadox." The resolution of this issue is important because rodents are so widely employed as surrogates for humans in genetic toxicology. This article will review the evolution in our understanding 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.

journal_name

Environ Mol Mutagen

authors

Hanawalt PC

doi

10.1002/em.1057

subject

Has Abstract

pub_date

2001-01-01 00:00:00

pages

89-96

issue

2-3

eissn

0893-6692

issn

1098-2280

pii

10.1002/em.1057

journal_volume

38

pub_type

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