XRCC1 and base excision repair balance in response to nitric oxide

► XRCC1 facilitates AAG-initiated BER OF ethenoadenine and hypoxanthine, key lesions that are induced by reactive nitrogen species (RNS). ► XRCC1 has a modest impact on sensitivity to RNS-induced genotoxicity. ► Overexpression of AAG renders XRCC1-deficient cells sensitive to RNS-induced DNA damage and toxicity. ► These data indicate that XRCC1 and AAG modulate RNS genotoxicity, and suggest that the impact of XRCC1 polymorphisms is dependent upon the level of AAG.