Abstract
Benzo[a]pyrene (B[a]P) is a member of the polycyclic aromatic hydrocarbons, compounds that are found in combustion products such as cigarette smoke and diesel exhaust and thought to be carcinogens capable of tumor initiation, promotion, and progression. B[a]P binds to the aryl hydrocarbon receptor (AhR) as a ligand and induces the expression of cytochrome P4501A1 (CYP1A1). Subsequently, B[a]P is metabolized by CYP1A1 to 7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE), which can eventually induce mutations or oxidative DNA damage. Research study In the present study, B[a]P has been exposed to endometrial adenocarcinoma cells (RL95-2) to investigate the potential cytotoxicological role of B[a]P in this cell type. The cells were cultured for 72 hrs in the medium containing 10% fetal bovine serum, and the various concentrations (0.01-100 uM) of B[a]P treatment revealed that significant cellular changes occurred from at 10 uM B[a]P during the treatment. B[a]P treatment caused increase of S phase in cell cycle and also reduced cell viability. Importantly, CYP1A1 protein and its activity were significantly elevated after B[a]P exposure, which indicates that B[a]P can be potentially converted into more cytotoxic forms (i.e., BPDE) in RL95-2 cells. The CYP1A1 was also localized in the cells by immunocytochemistry to confirm the protein expression in cellular level. Finally, α-naphtoflavone, a inhibitor of CYP1A1, treatment with B[a]P completely abolished the effect of B[a]P in the cells. These results suggest that B[a]P might be able to transduce its signal on endometrial cells by CYP1A1 activation.
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