Cancer cells differ from the other cells by their ability to survive under conditions of enhanced oxidative stress.
This property of cancer cells might also be an origin of resistance of tumors to drug treatment. Reactive oxygen species
(ROS) overproduction (oxidative stress) might be responsible for both survival and death of cancer cells and the opposite
effects of ROS signaling can depend on many reasons. In present work we consider several possible mechanisms of ROS
effects on survival/death cancer cells: the different effects of two main reactive oxygen species paramagnetic free radical
anion superoxide and diamagnetic molecule hydrogen peroxide, competition between protein kinases and phosphatases,
and modification of ROS-depended enzyme/gene cascades. The oxidation of protein kinase B (Akt) by ROS might be
of great importance for a shift of the survival to apoptotic signal in the enzymatic cascade. Dual effects of ROS
overproduction on cancer cells appear to depend on the levels of oxidative stress: weak/ moderate oxidative stress
enhances survival while severe oxidative stress induces cell death. The regulation of ROS overproduction by antioxidants
and prooxidants is possibly an important promising way for cancer treatment.
Keywords: ROS signaling, cancer, survival, apoptosis, diabetes mellitus, N-acetylcysteine, deetherification, deprotonation, glycolysis, cytochrome-cardiolipi
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