Fig 1.

Elevated-ROS cause nuclear DNA, thus leading to tumorigenesis. High levels of ROS oxidize adenine in DNA, thus leading to the formation of 8-oxo-dA and 2-OH-dA; in turn, 8-oxo-dA can lead to A→G and A→C mutations, and 2-OH-dA causes A→C, A→G, and A→T substitutions. ROS also oxidize guanine in DNA, resulting in the formation of 8-oxo-dG, which leads G→T transversion mutations. dGTP and dATP in the nucleotide pool are also oxidized by ROS, yielding 8-oxo-dGTP and 2-OH-dATP. The misincorporation of 8-oxo-dGTP and 2-OH-dATP as a substrate causes A→C and GC→AT mutation, respectively. Moreover, ROS impair the DNA damage repair system by downregulating the function of hOGG1 and BRCA2, thus leading to nuclear DNA mutations and favoring tumorigenesis. dATP, deoxyadenosine triphosphate; BRCA2, breast cancer susceptibility gene 2.