ABSTRACT
The Base Excision Repair (BER) pathway is responsible for repairing some of DNA’s most prevalent lesions-those produced both endogenously and exogenously from alkylation, oxidation, or spontaneous decomposition (e.g., deamination) of DNA bases (Izumi et al. 2003; Kelley et al. 2010; Vascotto and Fishel 2012). All forms of DNA damage alter its spatial confi guration, whether the helix is distorted or not. The BER pathway is the primary repair system involved in removing single damaged bases or abasic sites. Typically this corrective action occurs prior to replication in the cell cycle; otherwise, that damage could cause nucleotide mispairing or DNA strand breaks during replication (Mitra et al. 1997). Thus, effi cient repair helps to preserve genomic integrity. However, the repair process produces cytotoxic intermediates that must be resolved by completing repair swiftly
1Departments of Pediatrics and Pharmacology & Toxicology, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, 980 W. Walnut St. Walther Hall R3-C548, Indianapolis, IN 46202, USA. 2Department of Medical and Biological Sciences, University of Udine School of Medicine, P.le Kolbe 4, 33100, Udine, Italy. 3Betty and Earl Herr Professor in Pediatric Oncology Research, Departments of Pediatrics, Biochemistry & Molecular Biology, and Pharmacology & Toxicology, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, 980 W. Walnut St. Walther Hall R3-C528, Indianapolis, IN 46202, USA; Email: mkelley@iupui.edu *Corresponding author
and accurately; otherwise, accumulation of these intermediates can cause cell death (Guillet and Boiteux 2002).
