The production of 2-deoxyribonolactones (C1′-oxidation product), C4′-oxidized abasic sites and C5′-carbonyl terminated strand scission products was investigated in complexes of double-stranded DNA with protamine, poly-L-lysine and spermine exposed to X-ray radiation. The lesions were quantified by high-performance liquid chromatography through the release of the corresponding low-molecular-weight products 5-methylenefuran-2(5H)-one, N-(2′-hydroxy-ethyl)-5-methylene-D³-pyrrolin-2-one and furfural, respectively. All binders were found to increase the relative yield of C1′ oxidation up to 40% of the total 2-deoxyribose damage through the indirect effect versus approximately 18% typically found in homogeneous solutions by the same technique. On the contrary, the yield of C5′-oxidation was found to be suppressed almost completely, while in homogeneous solutions it constituted approximately 14% of the total. The observed change in end product distribution is attributed to free valence transfer to and from the complexing agent, although the mechanisms associated with this process remain unclear.