摘要
Manystudiesdemonstratethatconventionalanticancerdrugselevateintracellularlevelofreactiveoxygenspecies(ROS)andalterredox-homeostasisofcancercells.ItiswidelyacceptedthatanticancereffectofthesechemotherapeuticsisduetoinductionofoxidativestressandROS-mediatedapoptosisincancer.Ontheotherhand,theharmfulsideeffectsofconventionalanticancerchemotherapyarealsoduetoincreasedproductionofROSanddisruptionofredox-homeostasisofnormalcellsandtissues.ThisarticledescribesthemechanismsfortriggeringandmodulationofapoptosisthroughROS-dependentandROS-independentpathways.Wetrytoanswerthequestion:'Isitpossibletoinducehighlyspecificapoptosisonlyincancercells,withoutoverproductionofROS,aswellaswithoutharmfuleffectsonnormalcellsandtissues?'Thereviewalsosuggestsanewtherapeuticstrategyforselectivekillingofcancercells,withoutsignificantimpactonviabilityofnormalcellsandtissues,bycombininganticancerdrugswithredox-modulators,affectingspecificsignalingpathwaysandavoidingoxidativestress.
出版日期
2016年04月14日(中国期刊网平台首次上网日期,不代表论文的发表时间)