We have shown recently that halogenated quinones could enhance the decomposition of hydroperoxides and formation of alkoxyl/hydroxyl radicals independent of transition metal ions,and a nucleophilic substitution and homolytical decomposition reaction mechanism was proposed.However,neither the proposed quinone enoxy radical intermediate,nor the major reaction products were unambiguously identified.In the present study,one of the major reaction products between 2,5-dichloro-1,4-benzoquinone (DCBQ) and t-butylhydroperoxide (t-BuOOH) was identified as 2-hydroxy-3-t-butoxy-5-chloro-1,4-benzoquinone (CBQ(OH)-O-t-Bu),which is the rearranged isomer of the postulated quinone-peroxide reaction intermediate.The formation of CBQ(OH)-O-t-Bu was found to be inhibited by the spin trapping agent DMPO,and concurrently,a new DMPO adduct with one-chlorine isotope peak clusters at m/z 268 was observed.Further ESR spin-trapping,1H-NMR and HPLC/FTICR-MS studies with oxygen-17-labeled H2O2 strongly suggest that the radical trapped by DMPO is a carbon-centered quinone ketoxy radical,rather than the proposed oxygen-centered quinone enoxy radical.Analogous results were observed when DCBQ was substituted by other halogenated quinones.This study represents the first detection and identification of a novel quinone ketoxy radical,which provides direct experimental evidence to further support and expand our previously-proposed mechanism for metal-independent decomposition of hydroperoxides by halogenated quinones.Biological implications: Many widely-used biocides including chlorinated phenols,the Agent Orange and the brominated flame-retardant can be metabolized in vivo to di- or mono-halogenated quinones.Our data suggest that these halogenated quinones may react with hydroperoxides and exert toxic effects not only through enhanced production of alkoxyl/hydroxyl radicals,but also through the formation of carbon-centered quinone ketoxy radicals which may react directly with critical biological macromolecules such as DNA,protein and lipids.