Iron–anthracycline complex (null)

“Iron–anthracycline complexes” describes a chemical association between iron ions (typically Fe^2+ or Fe^3+) and anthracycline chemotherapy drugs such as doxorubicin or daunorubicin. These complexes play a crucial role in the mechanism of anthracycline-induced cardiotoxicity by catalyzing the formation of highly reactive oxygen species (particularly hydroxyl radicals) via redox cycling reactions. This oxidative stress damages DNA, lipids, and proteins, leading to myocardial cell injury and heart failure risk in patients treated with anthracyclines. Additionally, iron–anthracycline complexes interfere with cellular iron metabolism through effects on iron regulatory proteins, contributing further to cytotoxicity[2][3][4][7]. There is no evidence that the iron–anthracycline complex is itself a canonical therapeutic target like a receptor or enzyme, but rather it is a toxic species and mediator of adverse drug effects, with efforts made to block its formation (e.g., iron chelation with dexrazoxane) to protect the heart during chemotherapy[4][7][2].

Other names

Iron–doxorubicin complexIron–daunorubicin complexAnthracycline–iron complexIron–anthracycline redox complex

Generation of highly reactive free radicals via redox cycling (Fenton chemistry); Disruption of iron regulatory protein–iron response element (IRP–IRE) binding; Interference with iron-dependent cellular processes