Increasing the oxidative stress could be seen as increasing the genotoxic stress, this would be similar to using CPT, Etopo etc. drugs which increases the DNA damage and relying on healthy cells to repair the induced damage, is current part of cancer therapeutic strategy. I would also add that on the other hand tumour cells (which are defective in apoptosis commitment) could keep growing with increase genome instability and even increase tumorigenicity. This could be the reason why in cancer treatments they use combinations of drugs, which target more than one pathway
As any risk factor could be controll if oxidation time know. Should the proper frequency for oxidation at comparable in target genomic site? this may be the dillema in risk in drugs chronobiology. Second point is the principle of uncerntainty in physics law that the electron position or speed never simulteneus determine in deliver into cancer cell genomics. As exception to the uncertainty principle may be view in molecular bonding but atomic bonding?
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