Figure 1.

Unrepaired oxidative DNA damage can lead to cancer-promoting accumulation of mutations. Several stimuli from both endogenous and environmental sources induce increased production of ROS and RNI that can directly produce mutagenic DNA lesions. Oxidative DNA damage is primarily repaired by MMR repair and base excision repair pathways involving the excision of modified bases followed by repairing of the gaps. Oxidative DNA damage could exceed the repair capacity of these DNA repair pathways, or deficiency in these specific DNA repair pathways can lead to the accumulation of oncogenic mutations, precipitating cellular transformation and ultimately tumor initiation and/or progression.