Low-energy　electrons　(LEEs)　of　energies　≤30　eV　are　generated　in　large　quantities　by　ionizing　radiation.　These　electrons　can　damage　DNA;　particularly,　they　can　induce　the　more　detrimental　clustered　lesions　in　cells.　This　type　of　lesions,　which　are　responsible　for　a　large　portion　of　the　genotoxic　stress　generated　by　ionizing　radiation,　is　described　in　the　Introduction.　The　reactions　initiated　by　the　collisions　of　0.5–30　eV　electrons　with　oligonucleotides,　duplex　DNA,　and　DNA　bound　to　chemotherapeutic　platinum　drugs　are　explained　and　reviewed　in　the　subsequent　sections.　The　experimental　methods　of　LEE　irradiation　and　DNA　damage　analysis　are　described　with　an　emphasis　on　the　detection　of　cluster　lesions,　which　are　considerably　enhanced　in　DNA–Pt–drug　complexes.　Based　on　the　energy　dependence　of　damage　yields　and　cross-sections,　a　mechanism　responsible　for　the　clustered　lesions　can　be　attributed　to　the　capture　of　a　single　electron　by　the　electron　affinity　of　an　excited　state　of　a　base,　leading　to　the　formation　of　transient　anions　at　6　and　10　eV.　The　initial　capture　is　followed　by　electronic　excitation　of　the　base　and　dissociative　attachment—at　other　DNA　sites—of　the　electron　reemitted　from　the　temporary　base　anion.　The　mechanism　is　expected　to　be　universal　in　the　cellular　environment　and　plays　an　important　role　in　the　formation　of　clustered　lesions.　©　2019　by　the　authors.　Licensee　MDPI,　Basel,　Switzerland.