Oxidative Stress Biomarkers in Doxorubicin-Induced Multi-Organ Toxicity: Mechanisms, Clinical Relevance and Emerging Protective Strategies
Doxorubicin is an effective anthracycline used against solid and haematological malignancies, but dose-dependent multi-organ toxicity limits its clinical use. Oxidative stress is a major mechanism underlying this injury and produces measurable changes in redox biomarkers. This review synthesises evidence on mechanisms of doxorubicin-induced oxidative stress, major biomarkers, organ-specific patterns, clinical relevance and protective strategies. PubMed/MEDLINE, targeted Google Scholar searching and backward reference-list searching were used to identify literature from January 2010 to 10 August 2026. Relevant human, animal and in-vitro studies were considered, with seminal pre-2010 studies retained selectively for mechanistic context. Doxorubicin generally increases oxidative-damage markers, particularly malondialdehyde and 8-hydroxy-2′-deoxyguanosine, while reducing superoxide dismutase, catalase, glutathione peroxidase and glutathione. Evidence is strongest for cardiotoxicity, whereas clinical validation for non-cardiac organs is limited. Dexrazoxane and liposomal doxorubicin have stronger clinical evidence for cardioprotection, while many antioxidant and nanocarrier approaches remain preclinical. Oxidative-stress biomarkers are mechanistically informative but lack sufficient standardisation and prospective validation for routine predictive use. Integrated biomarker approaches require further clinical evaluation.