The aflatoxin B₁-induced formamidopyrimidine adduct is repaired by transcription-coupled nucleotide excision repair in human cells.

ABSTRACT: The mycotoxin, aflatoxin B₁ (AFB₁), is a potent mutagen that contaminates agricultural food supplies. After ingestion, AFB₁ is oxidized into a reactive electrophile that alkylates DNA, forming bulky lesions such as the genotoxic formamidopyrimidine lesion, AFB₁-Fapy dG. This lesion is mainly repaired by nucleotide excision repair (NER) in bacteria; however, in humans the picture is less clear. We report a plasmid-based host cell reactivation assay containing a site-specific AFB₁-Fapy dG lesion and present evidence that this lesion is mainly repaired by transcription-coupled NER (TC-NER) in human cells. Using a combination of isogenic knockout cell lines and immortalized fibroblasts from xeroderma pigmentosum and Cockayne syndrome patie

SUBMITTER: Laverty DJ 

PROVIDER: S-EPMC12409410 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature