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. Author manuscript; available in PMC: 2013 Feb 25.
Published in final edited form as: Toxicol Lett. 2011 Nov 30;209(1):58–66. doi: 10.1016/j.toxlet.2011.11.021

Fig. 1. Pathway of B[a]P Adduct Formation.

Fig. 1

Metabolism of the proximate carcinogen (−)-B[a]P-7,8-dihydrodiol to the ultimate carcinogen (+)-anti-B[a]PDE by CYP1A1/1B1 and to B[a]P-7,8-catechol by aldo-keto reductases of the 1C family. (+)-anti-trans-B[a]PDE is able to enter the nucleus and form the DNA-adduct (+)-anti-trans-B[a]PDE-dGuo. Alternatively, (+)-anti-trans-B[a]PDE can be detoxified through GST-mediated GSH adduct formation. B[a]P-7,8-catechol can redox cycle to B[a]P-7,8-dione, which generates reactive oxygen species that can cause oxidative DNA damage.