Iron Overload Pathophysiology and Antioxidant Therapeutics
Summary
Iron overload arises when regulatory mechanisms governing iron uptake, storage and excretion become overwhelmed, leading to excessive accumulation in vital organs such as the liver, heart and endocrine glands. Central to its pathophysiology is the catalytic role of free iron in the generation of reactive oxygen species via redox cycling, notably through Fenton and Haber–Weiss reactions. These processes precipitate lipid peroxidation, protein oxidation and DNA damage, culminating in cellular dysfunction, fibrosis and organ failure. Dysregulation of key hormones and transporters—hepcidin, ferroportin and transferrin—exacerbates iron deposition, while genetic disorders such as hereditary haemochromatosis and repeated transfusions in haematological diseases compound the burden. Antioxidant therapeutics encompass two principal approaches: iron chelation to deplete labile iron pools and antioxidant supplementation to bolster endogenous defences. Established chelators (deferoxamine, deferasirox) remain the bedrock of treatment, yet emerging strategies exploit natural compounds—polyphenols, flavonoids and oils—that both scavenge free radicals and modulate iron handling. Preclinical studies reveal that targeted antioxidants can restore superoxide dismutase and glutathione peroxidase activities, attenuate malondialdehyde formation and protect genomic integrity. Such interventions hold promise for reducing morbidity in thalassaemia, myelodysplastic syndromes and other iron‐loading conditions.
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Iron Overload Pathophysiology and Antioxidant Therapeutics publication trend
The graph below shows the total number of articles in iron overload pathophysiology and antioxidant therapeutics across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that can damage cellular components.
Fenton reaction: A chemical process in which ferrous iron reacts with hydrogen peroxide to produce hydroxyl radicals.
Lipid peroxidation: Oxidative degradation of lipids leading to cell membrane damage and formation of malondialdehyde.
Chelation: The binding of metal ions by organic ligands to form stable complexes, reducing free metal availability.
Hepcidin: A peptide hormone that regulates systemic iron homeostasis by controlling ferroportin‐mediated iron export.
References
- The effect of aqueous extract of Iranian oak (Quercus brantii) on lipid profile and liver enzymes in beta-thalassemia patients: a randomized controlled trial, double-blind, placebo-controlled. Frontiers in Nutrition (2025).
- Antioxidant Effects of Cactus Seed Oil against Iron-Induced Oxidative Stress in Mouse Liver, Brain and Kidney. Molecules (2024).
- α-Lipoic Acid Reduces Iron-induced Toxicity and Oxidative Stress in a Model of Iron Overload. International Journal of Molecular Sciences (2019).
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