简介：Manystudiesdemonstratethatconventionalanticancerdrugselevateintracellularlevelofreactiveoxygenspecies(ROS)andalterredox-homeostasisofcancercells.ItiswidelyacceptedthatanticancereffectofthesechemotherapeuticsisduetoinductionofoxidativestressandROS-mediatedapoptosisincancer.Ontheotherhand,theharmfulsideeffectsofconventionalanticancerchemotherapyarealsoduetoincreasedproductionofROSanddisruptionofredox-homeostasisofnormalcellsandtissues.ThisarticledescribesthemechanismsfortriggeringandmodulationofapoptosisthroughROS-dependentandROS-independentpathways.Wetrytoanswerthequestion:'Isitpossibletoinducehighlyspecificapoptosisonlyincancercells,withoutoverproductionofROS,aswellaswithoutharmfuleffectsonnormalcellsandtissues?'Thereviewalsosuggestsanewtherapeuticstrategyforselectivekillingofcancercells,withoutsignificantimpactonviabilityofnormalcellsandtissues,bycombininganticancerdrugswithredox-modulators,affectingspecificsignalingpathwaysandavoidingoxidativestress.
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