**3.2 Oxidative stress**

130 Selected Topics in DNA Repair

Fig. 3. Aryl hydrocarbon receptor (AhR) pathway activated by BaP induces expression of

*cyp1A1* and *cyp1B1*.

It has been reported that BaP derivatives have the capacity to enter redox cycles and induce the production of reactive oxygen species (ROS), thereby causing oxidative stress (An, et al., 2011). BaP radical-cations are precursors for 6-OH-BaP. Auto-oxidation of this derivative may result in the formation of BaP quinones such as 6, 12-, 1,6- and 3,6-BaP dione (Briede, et al., 2004). These metabolites can undergo redox-cycling to their corresponding BaP diols and produce superoxide reactive oxygen species which are then converted to hydroxyl radicals by the Haber-Weiss reaction (Lesko & Lorentzen, 1985). Free radicals react with guanine and cause DNA damage, including the production of 7-hydro-8-oxo-20-deoxyguanosine (8-oxodG) (Chatgilialoglu & O'Neill, 2001). The OGG1 gene codes for a DNA glycosylase involved in base excision repair of 8-oxo-dG that arises from ROS. When this system fails there is an increase in mutation rate (Bonner, et al., 2005). Balance between generation of ROS species and scavenging of these molecules is fundamental in repairing DNA damage. If the rate of ROS generation is greater than their removal it is likely that more DNA damage will result. PAHs may absorb light energy in UVR (280–400 nm) region and may induce DNA damage by production of ROS. For example, chrysene, induces apoptosis and DNA damage in human keratinocytes by generating ROS in response to UVB radiation (Ali, et al., 2011).
