Bisphenol compounds (BPs) are ubiquitously existing pollutants. Recent evidence shows that they’re going to be activated by human CYP1A1 for clastogenic effects however, factors that influence/mediate CYP1A1-activated 4,4′-(hexafluoroisopropylidene)diphenol (BPAF) toxicity, specially the aryl hydrocarbon receptor (AhR), sulfotransferase (SULT) 1A1 [recognized to conjugate 2,2-bis(4-hydroxyphenol)-lp (BPA)] and reactive oxygen species (ROS), remain unclear. Within this study, an individual hepatoma (HepG2) cell line was genetically engineered for that expression of human CYP1A1 and SULT1A1, producing HepG2-hCYP1A1 and HepG2-hSULT1A1, correspondingly. They were utilized in the micronucleus make sure |?-H2AX analysis (Western blot) (indicating double-strand DNA breaks) with BPAF the function of AhR in mediating BPAF toxicity was investigated by coexposure of AhR modulators in HepG2 and it is derivative C3A (without any genetic modifications but enhanced CYP expression). The outcomes indicated induction of micronuclei by BPAF (?Y 2.5 |ìM, for just two-cell cycle) in HepG2-hCYP1A1 and C3A, while inactive in HepG2 and HepG2-hSULT1A1 however, BPAF caused micronuclei in HepG2 pretreated with 3,3′,4,4′,5-pentachlorobiphenyl (PCB126, AhR activator), and BAY-218 (AhR inhibitor) blocked the result of BPAF in C3A. In HepG2-hCYP1A1 BPAF selectively caused centromere-free micronuclei (immunofluorescent assay) and double-strand DNA breaks. In HepG2 cells receiving conditional medium from BPAF-HepG2-hCYP1A1 incubation micronuclei were created, while negative in HepG2-hSULT1A1. Finally, the intracellular amounts of ROS, superoxide dismutase and reduced glutathione in C3A and HepG2-hCYP1A1 uncovered to BPAF counseled me moderately elevated, while unchanged in HepG2 cells. To conclude, like other BPs BPAF is activated by human CYP1A1 for potent clastogenicity, which effect is enhanced by AhR while alleviated by SULT1A1.