Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review

Cancer therapy-related cardiotoxicity has emerged as a major challenge in contemporary oncology, particularly in long-term survivors of childhood malignancies. Oxidative stress (OS)-induced cardiotoxicity represents a key mechanistic pathway underlying myocardial injury caused by numerous anti-neoplastic drugs, most notably anthracycline-based chemotherapy, while OS also critically contributes to radiotherapy-induced cardiotoxicity. Excessive reactive oxygen and nitrogen species generation promotes mitochondrial dysfunction, impaired calcium homeostasis, lipid peroxidation, endothelial injury, inflammatory activation, and cardiomyocyte apoptosis, ultimately leading to progressive cardiac remodeling and ventricular dysfunction. These processes are of particular concern in pediatric cancer survivors, especially children treated for leukemia, who face a substantially elevated lifetime risk of cardiovascular disease following treatment exposure. Increasing attention has, therefore, been directed toward nutritional strategies capable of modulating redox homeostasis and attenuating treatment-associated myocardial injury. Experimental and translational evidence suggests that selected dietary compounds and nutraceuticals, including polyphenols, omega-3 fatty acids, coenzyme Q10, selenium, antioxidant vitamins, nutrition-based epigenetic interventions and intestinal microbiota composition modulations may exert cardioprotective effects through preservation of mitochondrial integrity, enhancement of endogenous antioxidant defenses, and suppression of oxidative and inflammatory signaling pathways. Nevertheless, clinical implementation remains limited by insufficient standardization, heterogeneous study designs, and incomplete understanding of long-term efficacy and safety. This narrative review critically examines the molecular basis of the OS-induced cardiotoxicity and radiotherapy-induced cardiotoxicity and evaluates current evidence supporting nutrition-based cardioprotective interventions, with particular emphasis on pediatric leukemia survivors and the prevention of long-term cardiovascular complications following anticancer therapy.