Figure 1.

Accumulation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS), derived either endogenously or exogenously, results in oxidative stress. Disruption of thiol and non-radical circuits may also result in oxidative stress. The extent of this stress will either result in lethal damage and apoptosis or in cell adaptation. In cancer cells chronic oxidative stress activates redox sensitive transcription factors and signaling pathways that act to increase the expression of antioxidants, increase expression of survival factors as well inhibit the expression of pro-apoptotic pathways. ROS/RNS induced DNA injury promotes genomic instability and further provides opportunity to adapt to oxidative stress. Cancer progression occurs via the regulation of redox dependent expression of genes that play roles in proliferation, senescence evasion, metastasis, and angiogenesis. These features in association with the disruption in antioxidant profile may contribute to altered drug sensitivity and chemotherapy resistance. Definition of abbreviations: NOX, NADPH oxidase; nuclear factor-κB; NF-κB; Cys, cysteine; Cyss; cystine; GSH, glutathione; GSSH, glutathione disulfide, GSTP, glutathione-S-transferase P