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. Author manuscript; available in PMC: 2015 Sep 15.
Published in final edited form as: Mutat Res Genet Toxicol Environ Mutagen. 2014 Aug 7;0:34–41. doi: 10.1016/j.mrgentox.2014.07.010

Figure 1. Metabolism of Benzo[a]pyrene (BaP).

Figure 1

The metabolism primarily occurs via cytochrome P450s (CYP1A1 and CYP1B1), peroxidases (epoxide hydrolase) and aldo-keto reductase. The major metabolite which is thought to cause carcinogenesis is BaP-7,8-diol-9,10-epoxide (BPDE) which is metabolised via BaP-7,8-epoxide and BaP-7,8-diol. BPDE forms DNA-adducts which can induce G→T transversions. In addition, many metabolites (such as catechol and dione within a futile cycle) form reactive oxygen species (ROS) thus adding to oxidative stress and contributing to the formation of oxidative DNA lesions such as 8-oxoguanine, a pre-mutagenic DNA lesion. Radical cations are formed in a minor quantity.