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. Author manuscript; available in PMC: 2015 Oct 15.
Published in final edited form as: Mol Nutr Food Res. 2011 Jun 29;55(9):1291–1300. doi: 10.1002/mnfr.201100148

Figure 8.

Figure 8

Lack of repair of Acr-induced DNA damage in the p53 gene (A) as well as in genome overall (B) in normal human NER proficient NHLF (CCL-202) and NER deficient XPA cells. Exponentially growing cells at 70% confluency were treated with Acr (100 μM) for 6 h, then incubated in fresh medium without Acr for 0, 2, 4, and 8 h. The genomic DNAs were isolated and reacted with UvrABC which can cut Acr-dG adducts [9, 11]. Acr-DNA adducts formed in exon 7 of the p53 gene were mapped at the nucleotide level by the UvrABC-LMPCR method as previously described [9]. Note: Acr-DNA adducts were not repaired at the genome level and at the codons 244, 248 and 249 of the p53 gene.