Chemoradiation　therapy　(CRT),　which　combines　a　chemotherapeutic　drug　with　ionizing　radiation　(IR),　is　the　most　common　cancer　treatment.　At　the　molecular　level,　the　binding　of　Pt-drugs　to　DNA　sensitizes　cancer　cells　to　IR,　mostly　by　increasing　the　damage　induced　by　secondary　low-energy　(0-20　eV)　electrons　(LEEs).　We　investigate　such　enhancements　by　binding　terpyridine-platinum　(Tpy-Pt)　to　supercoiled　plasmid　DNA.　Fifteen　nanometer　thick　films　of　Tpy-Pt-DNA　complexes　in　a　molar　ratio　of　5　:　1　were　irradiated　with　monoenergetic　electrons　of　5　and　10　eV,　which　principally　attach　to　the　DNA　bases　to　form　transient　anions　(TAs)　decaying　into　a　multitude　of　bond-breaking　channels.　At　both　energies,　the　effective　yields　of　crosslinks　(CLs),　base　damage　(BD)　related　CLs,　single　and　double　strand　breaks　(SSBs　and　DSBs),　non-DSB-cluster　lesions,　loss　of　supercoiled　configuration　and　base　lesions　are　6.5　±　1.5,　8.8±　3.0,　88　±　11,　5.3　±　1.3,　9.6　±　2.2,　106　±　17,　189　±　31　×　10−15　per　electron　per　molecule,　and　11.9　±　2.6,　19.9　±　4.4,　128　±　18,　7.7　±　3.0,　13.4　±　3.9,　144　±　19,　229　±　42　×　10−15　per　electron　per　molecule,　respectively.　DNA　damage　increased　1.2-4.2-fold　due　to　Tpy-Pt,　the　highest　being　for　BD-related　CLs.　These　enhancements　are　slightly　higher　than　those　obtained　by　the　conventional　Pt-drugs　cisplatin,　carboplatin　and　oxaliplatin,　apart　from　BD-related　CLs,　which　are　about　3　times　higher.　Enhancements　are　related　to　the　strong　perturbation　of　the　DNA　helix　by　Tpy-Pt,　its　high　dipole　moment　and　its　favorable　binding　to　guanine　(G),　all　of　which　increase　bond-breaking　via　TA　formation.　In　CRT,　Tpy-Pt　could　considerably　enhance　crosslinking　within　genomic　DNA　and　between　DNA　and　other　components　of　the　nucleus,　causing　roadblocks　to　replication　and　transcription,　particularly　within　telomeres,　where　it　binds　preferentially　within　G-quadruplexes.　©　2023　The　Royal　Society　of　Chemistry.