Ferroptosis is a form of non-apoptotic cell death characterized by phospholipid peroxidation promoted by iron-dependent radical reactions. Glutathione peroxidase 4 (GPX4) is a key enzyme that protects phospholipids from peroxidation and suppresses ferroptosis. The dysregulation of genes involved in cysteine and glutathione metabolism is closely associated with ferroptosis. Active proliferation cells are more prone to ferroptosis than quiescent cells, suggesting that radical species generated during oxygen-involved metabolism are responsible for lipid peroxidation. This review discusses the initial events of ferroptosis, focusing on energy metabolism and cysteine deficiency. Mitochondria are likely sources of both radical electrons and free iron, and their dysfunction can lead to lipid peroxidation. The review also explores the role of nitrogen metabolism in ferroptosis, including the urea cycle and polyamine pathways. Additionally, it highlights the importance of the redox system in suppressing ferroptosis, particularly through the actions of GPX4 and other enzymes.Ferroptosis is a form of non-apoptotic cell death characterized by phospholipid peroxidation promoted by iron-dependent radical reactions. Glutathione peroxidase 4 (GPX4) is a key enzyme that protects phospholipids from peroxidation and suppresses ferroptosis. The dysregulation of genes involved in cysteine and glutathione metabolism is closely associated with ferroptosis. Active proliferation cells are more prone to ferroptosis than quiescent cells, suggesting that radical species generated during oxygen-involved metabolism are responsible for lipid peroxidation. This review discusses the initial events of ferroptosis, focusing on energy metabolism and cysteine deficiency. Mitochondria are likely sources of both radical electrons and free iron, and their dysfunction can lead to lipid peroxidation. The review also explores the role of nitrogen metabolism in ferroptosis, including the urea cycle and polyamine pathways. Additionally, it highlights the importance of the redox system in suppressing ferroptosis, particularly through the actions of GPX4 and other enzymes.