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Figure 1 | BMC Cancer

Figure 1

From: Immunohistochemical analysis of oxidative stress and DNA repair proteins in normal mammary and breast cancer tissues

Figure 1

Role of oxidative stress and DNA repair proteins in cells. NM23-H1 induced DNA nicks may lead to DNA repair or apoptosis. Endogenous or exogenous alkylating agents cause DNA lesions such as 3-methylguanine (3-MeG), which are recognized and removed by MPG and leave apurinic sites. Ape1/Ref-1 recognizes apurinic sites and cleaves the adjacent DNA backbone. DNA repair can be completed through the base excision repair pathway. If not repaired, apurinic sites can result in double-stranded breaks. γ-H2AX associates with double-stranded breaks and recruits DNA repair proteins. Reactive oxygen species (ROS), which include superoxide (O2 –·), hydrogen peroxide (H2O2), and hydroxyl radical (OH·), are formed as byproducts of normal cellular metabolism and can produce DNA lesions such as 8-OxoG, which are excised by cellular DNA glycosylases. Accumulated O2 interacts with nitric oxide (NO·) to produce peroxynitrite (OONO–), which in turn nitrates tyrosines and alters protein structure/function. TrxR uses NADPH to reduce Trx, which in turn reduces and activates Ape1/Ref-1. Activated Ape1/Ref-1 reduces a number of proteins including various transcription factors.

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