Articles

Ferroptosis is a non-necrotic, iron-dependent cell death that is caused by lipid peroxidation overload and antioxidant defenses breakdowns. In comparison to apoptosis or necrosis, ferroptosis is developed because of metabolic vulnerabilities, especially iron imbalances, glutathione deficiency, glutathione peroxidase 4 suppression and phospholipid oxidation. Nutritional conditions have been identified as potent regulators of ferroptotic susceptibility since diet affects antioxidant stores, membrane lipids, redox metabolism and iron condition. This review identically describes the biochemical processes involved in ferroptosis, particularly the role of iron redox cycling, polyunsaturated fatty acid peroxidation, antioxidant enzyme and other lipid repair pathways. It also discusses the role of nutrients like selenium, vitamin E, Coenzyme Q10, sulfur related amino acids, iron and dietary fatty acids in the regulation of ferroptotic signaling. Lastly, biological usefulness of ferroptosis in humans and animals is addressed, including its role in cancer biology, neurodegeneration, infectious disease, metabolic diseases and veterinary diseases. Nutritional management is suggested as the potential solution to tune ferroptosis for improving health and preventing tissue damage and increasing resilience to disease.