Abstract
Human cancer can be initiated by DNA damage caused by UV, ionizing radiation, and environmental chemical agents (Gundy 2006). To safeguard the integrity of genomes, humans have developed a set of complex DNA repair systems. Among the five main DNA maintenance mechanisms operating in mammals, base excision repair is the primary guardian against damage that results from cellular metabolism, including reactive oxygen species, methylation, deamination, and hydroxylation (Cheadle and Sampson 2003). Therefore, base excision repair is a universal event in cells and is relevant for preventing mutagenesis. The X-ray repair cross-complementary 1 (XRCC1) gene product is implicated in single-strand break repair and base excision repair mechanisms (Kubota et al. 1996; Xing et al. 2002). The XRCC1 protein interacts with poly (ADP-ribose) polymerase, DNA polymerase b, and DNA ligase IIIa, participating in multistep base excision repair and removal of base adducts produced by oxidative damage, methylation, reduction, or fragmentation (Caldecott et al. 1996; Cappelli et al. 1997; Kubota et al. 1996). Cells with a mutant XRCC1 gene have increased sensitivity to ultraviolet or ionizing radiation and alkylating agents (Brem and Hall 2005). Three important polymorphisms leading to amino acid substitutions have been identified at the evolutionarily conserved regions of the XRCC1 gene (Shen
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