scholarly journals Adenine–DNA Adducts Derived from the Highly Tumorigenic Dibenzo[a,l]pyrene Are Resistant to Nucleotide Excision Repair while Guanine Adducts Are Not

2013 ◽  
Vol 26 (5) ◽  
pp. 783-793 ◽  
Author(s):  
Konstantin Kropachev ◽  
Marina Kolbanovskiy ◽  
Zhi Liu ◽  
Yuqin Cai ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Dna Adducts ◽  
Excision Repair ◽  
Nucleotide Excision ◽  
Guanine Adducts

scholarly journals Base pair conformation-dependent excision of benzo[a]pyrene diol epoxide-guanine adducts by human nucleotide excision repair enzymes.

1997 ◽  
Vol 17 (12) ◽  
pp. 7069-7076 ◽  
Author(s):  
M T Hess ◽  
D Gunz ◽  
N Luneva ◽  
N E Geacintov ◽  
H Naegeli
Keyword(s):  
Nucleotide Excision Repair ◽  
Dna Adducts ◽  
Excision Repair ◽  
Dna Conformation ◽  
Repair Processes ◽  
Repair Enzymes ◽  
Diol Epoxide ◽  
Nucleotide Excision ◽  
Guanine Adducts ◽  
Repair Activity

Human nucleotide excision repair processes carcinogen-DNA adducts at highly variable rates, even at adjacent sites along individual genes. Here, we identify conformational determinants of fast or slow repair by testing excision of N2-guanine adducts formed by benzo[a]pyrene diol epoxide (BPDE), a potent and ubiquitous mutagen that induces mainly G x C-->T x A transversions and frameshift deletions. We found that human nucleotide excision repair processes the predominant (+)-trans-BPDE-N2-dG adduct 15 times less efficiently than a standard acetylaminofluorene-C8-dG lesion in the same sequence. No difference was observed between (+)-trans- and (-)-trans-BPDE-N2-dG, but excision was enhanced about 10-fold by changing the adduct configurations to either (+)-cis- or (-)-cis-BPDE-N2-dG. Conversely, excision of (+)-cis- and (-)-cis- but not (+)-trans-BPDE-N2-dG was reduced about 10-fold when the complementary cytosine was replaced by adenine, and excision of these BPDE lesions was essentially abolished when the complementary deoxyribonucleotide was missing. Thus, a set of chemically identical BPDE adducts yielded a greater-than-100-fold range of repair rates, demonstrating that nucleotide excision repair activity is entirely dictated by local DNA conformation. In particular, this unique comparison between structurally highly defined substrates shows that fast excision of BPDE-N2-dG lesions is correlated with displacement of both the modified guanine and its partner base in the complementary strand from their normal intrahelical positions. The very slow excision of carcinogen-DNA adducts located opposite deletion sites reveals a cellular strategy that minimizes the fixation of frameshifts after mutagenic translesion synthesis.

scholarly journals Lack of recognition by global-genome nucleotide excision repair accounts for the high mutagenicity and persistence of aristolactam-DNA adducts

2011 ◽  
Vol 40 (6) ◽  
pp. 2494-2505 ◽  
Author(s):  
Victoria S. Sidorenko ◽  
Jung-Eun Yeo ◽  
Radha R. Bonala ◽  
Francis Johnson ◽  
Orlando D. Schärer ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Dna Adducts ◽  
Excision Repair ◽  
Nucleotide Excision
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